- Thứ ba, 30 Tháng 8 2016 14:52
Tháng 5/2016, ESC đã đưa ra Hướng dẫn cho chẩn đoán và điều trị suy tim cấp và mạn tính. Chúng tôi xin tóm tắt cập nhật này về phương diện điều trị rối loạn nhịp ở bệnh nhân suy tim, trong đó có điều trị bằng dụng cụ không phẫu thuật và điều trị bằng thuốc.
TS Phạm Hữu Văn
ThS Lê Thị Xuân Thúy
Để cho các đồng nghiệp tiện theo dõi chúng tôi xin lược qua về một số khái niệm có tính cập nhật cao về suy tim trước khi trình bày cụ thể theo mục đích của bài viết này. Chúng tôi vẫn lấy số các mục thứ tự theo đúng như Khuyến cáo để các đồng nghiệp có thể tiện tham khảo thêm các phần khác của Khuyến cáo nguyên bản.
Mục đích của tất cả các hướng dẫn của ESC là giúp các chuyên gia y tế đưa ra quyết định dựa trên những bằng chứng tốt nhất. Chúng ta sẽ sớm được ăn mừng kỷ niệm 30 năm về thử nghiệm lâm sàng đầu tiên chứng minh rằng hậu quả tồi tệ của suy tim (HF) đối với bệnh nhân có thể được cải thiện rõ rệt. [2] Kể từ đó, trong lĩnh vực điều trị HF, chúng ta đã chứng kiến và ghi nhớ nhiều thành tựu vượt trội, cho phép chúng ta làm sáng tỏ sinh lý bệnh của hội chứng lâm sàng này, mà quan trọng hơn là chúng ta tìm được cách chăm sóc tốt hơn các bệnh nhân của mình. [3] Tới năm 2016, không ai còn có thể phản bác điều hiển nhiên là: bằng cách áp dụng tất cả những khám phá dựa trên bằng chứng, HF giờ trở thành một căn bệnh có thể phòng ngừa và điều trị được.
Mục đích của tài liệu này là để cung cấp các hướng dẫn dựa trên bằng chứng thực tế cho việc chẩn đoán và điều trị suy tim. Những thay đổi chủ yếu từ các hướng dẫn năm 2012 liên quan đến:
- Thuật ngữ mới cho bệnh nhân suy tim và phân suất tống máu thất trái (LVEF) ở khoảng 40-49% - 'HF với EF mức chung bình (HFmrEF)'; Người ta tin rằng việc xác định HFmrEF như một nhóm riêng biệt sẽ kích thích nghiên cứu về các đặc trưng cơ bản, sinh lý bệnh và điều trị của quần thể này.
- Các khuyến cáo rõ ràng về tiêu chuẩn chẩn đoán HF với EF giảm (HFrEF), HF với EF giảm trung bình (HEmrEF) và HF EF bảo tồn (HFpEF).
- Mô hình thuật toán mới để chuẩn đoán HF trong trạng thái không cấp trên cơ sở đánh giá khả năng HF.
- Các khuyến cáo hướng vào ngăn ngừa hoặc làm chậm sự phát triển của HF được biểu hiện hoặc ngăn ngừa tử vong trước khi khởi phát triệu chứng.
- Chỉ định sử dụng phối hợp thuốc mới sacubitril/valsartan, đầu tiên ở class của ARNIs (angiotensin receptor neprilysin inhibitors).
- Các chỉ định sửa đổi cho CRT (cardiac resynchronization therapy)
- Nguyên tắc khởi đầu sớm điều trị phù hợp tiếp tục cùng với các phát hiện liên quan trong HF cấp tiếp theo cách tiếp cận 'thời gian để điều trị' đã được thành lập trong hội chứng mạch vành cấp (ACS).
- Thuật toán mới cho chẩn đoán và tiếp cận điều trị phối hợp HF cấp trên cơ sở có /không có ứ huyết/ giảm tưới máu.
Người ta đi theo định dạng các Hướng dẫn HF của ESC 2012 trước. Các khuyến cáo điều trị nêu tác dụng điều trị hỗ trợ bằng các class độ mạnh và mức độ bằng chứng của khuyến cáo trong các định dạng bảng; trong trường hợp suy tim mạn tính do rối loạn chức năng tâm thu thất trái (LVSD) các khuyến cáo tập trung vào kết quả tử suất và bệnh suất. Các tóm tắt chi tiết về các bằng chứng quan trọng hỗ trợ cho phương pháp điều trị thường được khuyến cáo đã được cung cấp. Đối với các khuyến cáo chẩn đoán mức độ bằng chứng C đã được quyết định một cách cơ bản, do phần lớn các test chẩn đoán không có số liệu từ các nghiên cứu ngẫu nhiên (RCT) cho thấy chúng sẽ hướng đến giảm bệnh suất và hoặc tử suất. Hướng dẫn thực hành được cung cấp cho việc sử dụng các thuốc lợi tiểu và các thuốc làm thay đổi bệnh quan trọng. Khi có thể, các hướng dẫn có liên quan khác, các tuyên bố đồng thuận và các văn bản thể hiện quan điểm đã được trích dẫn để tránh văn bản quá dài. Tất cả các bảng phải được đọc cùng với văn bản đi kèm của chúng và không đọc trong sự đơn độc.
3.1 Khái niệm suy tim
HF là một hội chứng lâm sàng đặc trưng bằng các triệu chứng điển hình (ví dụ như khó thở, phù mắt cá chân và mệt mỏi), có thể kèm theo các dấu hiệu (ví dụ như tăng áp lực tĩnh mạch cảnh, ran ẩm ở phổi và phù ngoại vi) gây ra do sự bất thường cấu trúc và / hoặc chức năng của tim, dẫn đến giảm cung lượng tim và/hoặc áp lực trong tim cao lúc nghỉ hoặc trong quá trình căng thẳng.
Các định nghĩa hiện tại của HF giới hạn tự bản thân nó đối với các giai đoạn trong đó các triệu chứng lâm sàng là biểu hiện bên ngoài. Trước khi các triệu chứng lâm sàng biểu hiện, bệnh nhân có thể biểu hiện các bất thường cấu trúc hoặc chức năng không triệu chứng [rối loạn chức năng tâm thu hoặc tâm trương thất trái (LV)], đó là điểm báo trước (precursors) của HF. Ghi nhận các điểm báo trước này là quan trọng do chúng có liên quan đến hậu quả xấu, bắt đầu điều trị ở giai đoạn điểm báo trước có thể làm giảm tỷ lệ tử vong ở bệnh nhân có rối loạn chức năng LV tâm thu không có triệu [4, 5].
Minh chứng một nguyên nhân tim cơ bản là trung tâm để chẩn đoán suy tim. Đây thường là sự bất thường cơ tim gây ra rối loạn chức năng tâm thu thất và/hoặc tâm trương. Tuy nhiên, sự bất thường của van, màng ngoài tim, màng trong tim, nhịp tim và dẫn truyền cũng có thể gây ra suy tim (và nhiều hơn một sự bất thường thường có). Xác định các vấn đề tim cơ bản là rất quan trọng đối với lý do chữa bệnh, khi bệnh lý chính xác xác định điều trị cụ thể được sử dụng (ví dụ sửa van hoặc thay thế cho bệnh van tim, điều trị dược lý cụ thể đối với HF với giảm EF, giảm nhịp tim trong bệnh cơ tim do nhịp nhanh, v.v).
3.2 Thuật ngữ học
3.2.1 Suy tim với phân suất bảo tồn, mức độ trung bình và giảm(Heart failure with preserved, mid-range and reduced ejection fraction)
Các thuật ngữ chính được sử dụng để mô tả HF là bệnh sử và được dựa trên cơ sở đo LVEF. HF bao gồm một phạm vi biên đổi rộng các bệnh nhân, từ những người có LVEF bình thường [thường coi là ≥50%; HF với EF bảo tồn (preserved) (HFpEF)] với những người có giảm LVEF [thường coi là <40%; HF với giảm EF (HFrEF)] (Bảng 3.1). Bệnh nhân có LVEF trong khoảng 40-49% đại diện cho một "vùng xám", vùng này bây giờ chúng ta định nghĩa như HFmrEF (Bảng 3.1). Sự khác biệt của bệnh nhân suy tim dựa trên LVEF rất quan trọng do bệnh căn cơ bản khác biệt, nhân khẩu học, có bệnh kèm theo và đáp ứng với liệu pháp khác nhau.[6] Hầu hết các thử nghiệm lâm sàng được xuất bản sau năm 1990 bệnh nhân được lựa chọn dựa trên LVEF [thường được đo bằng siêu âm tim, kỹ thuật hạt nhân phóng xạ hoặc cộng hưởng từ tim (CMR)], và chỉ ở những bệnh nhân với HFrEF, phương pháp điều trị đã được chứng minh làm giảm tử suất và bệnh suất.
Bảng 3.1. Định nghĩa suy tim với bảo tồn (HFpEF), phạm vi nhẹ (HFmrEF) và phân suất tống máu giảm (HFrEF)
Type HF
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HFrEF
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HFmrEF
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HFpEF
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Criteria
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1
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Triệu chứng ± dấu hiệua
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Triệu chứng ± dấu hiệua
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Triệu chứng ± dấu hiệua
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2
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LVEF < 40%
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LVEF: 40 - 49%
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LVEF ≥ 50%
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3
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-
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1.Mức độ natruretic peptide tăng lênb.
2. Ít nhất một tiêu chuẩn bổ xung:
a. Bệnh tim thực thể thích hợp (LVH và hoặc LAE)
b. Rối loạn chức năng tâm trương (xem chi tiết mục 4.3.2)
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1.Mức độ natruretic peptide tăng lênb.
2. Ít nhất một tiêu chuẩn bổ xung
a. Bệnh tim thực thể thích hợp (LVH và hoặc LAE)
b. Rối loạn chức năng tâm trương (xem chi tiết mục 4.3.2)
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BNP: B-type natriuretic peptide. HFrEF: heart failure. HFmrEF: heart failure mid range ejection fraction. HFrEF: heart failure reduced ejection fraction. HEpEF: heart failure preserved ejection fraction. LVEF: left ventricular ejection fraction. LAE: left atrial enlargement. NT- proBNP: N-terminal pro - B-type natriuretic peptide.
aDấu hiệu có thể không biểu hiện ở các giai đoạn sớm của suy tim (đặc biệt suy tim EF còn bù), bệnh nhân được điều trị lợi tiểu.
bBNP> 35pg/ml hoặc Nt proBNP > 125pg/ml
Chẩn đoán HFpEF thách thức lớn hơn so với chẩn đoán HFrEF. Bệnh nhân HFpEF thường không có giãn LV, nhưng thay vào đó thường có sự gia tăng độ dày thành LV và / hoặc kích thước nhĩ trái tăng lên (LA) như một dấu hiệu của sự gia tăng áp lực đổ đầy. Hầu hết có thêm "bằng chứng" đổ đầy LV hoặc khả năng hút suy giảm, cũng được xếp vào loại rối loạn chức năng tâm trương, thường được chấp nhận như là nguyên nhân gây ra suy tim ở những bệnh nhân này (do đó thuật ngữ "HF tâm trương"). Tuy nhiên, hầu hết bệnh nhân HFrEF (trước đây được gọi là " HF tâm thu") cũng có rối loạn chức năng tâm trương và bất thường tinh tế của chức năng tâm thu đã được thể hiện ở những bệnh nhân HFpEF. Do đó ưu tiên cho tình trạng LVEF bảo tồn hoặc LVEF giảm qua việc "chức năng tâm thu" bảo tồn hay giảm.
Trong các hướng dẫn trước người ta đã thừa nhận "vùng màu xám" (grey area) tồn tại giữa HFrEF và HFpEF. [7] Các bệnh nhân này có LVEF phạm vi từ 40 đến 49%, do đó có thuật ngữ HF mức độ nhẹ (HFmrEF). Xác định HFmrEF như một nhóm riêng biệt sẽ kích thích nghiên cứu về các đặc trưng cơ bản, sinh lý bệnh và điều trị các bệnh nhân nhóm bệnh này. Các bệnh nhân HFmrEF nhiều khả năng nhất có rối loạn chức năng tâm thu nhẹ là chủ yếu, nhưng với các đặc trưng của rối loạn chức năng tâm trương (Bảng 3.1).
Bệnh nhân có bệnh cơ tim LV không được phát hiện có thể có các nguyên nhân tim mạch khác cho HF (ví dụ tăng huyết áp phổi, bệnh van tim, vv). Bệnh nhân có các bệnh lý không phải lý tim mạch (thiếu máu, bệnh phổi, bệnh thận hoặc gan) có thể có các triệu chứng tương tự hoặc giống hệt với HF và mỗi thể làm phức tạp hoặc làm trầm trọng thêm các triệu chứng suy tim.
3.2.2 Thuật ngữ học liên quan đến các quá trình thời gian suy tim
Trong hướng dẫn này, các HF hạn được sử dụng để mô tả các hội chứng có triệu chứng, phân loại theo Hiệp hội Tim mạch New York (NYHA) phân loại chức năng (xem Phần 3.2.3 và trang Web Bảng 3.2), mặc dù bệnh nhân có thể được trở lại không có triệu chứng bằng điều trị. Trong hướng dẫn này, bệnh nhân đã không bao giờ biểu hiện các triệu chứng điển hình và / hoặc dấu hiệu của suy tim và với giảm LVEF được mô tả như rối loạn LV tâm thu không có triệu chứng. Các bệnh nhân đã có HF trong thời gian nào đó thường được cho là có “HF mạn tính". Một bệnh nhân được điều trị với các triệu chứng và dấu hiệu đó vẫn thường không thay đổi trong ít nhất 1 tháng được cho là 'dai dẳng' (stable). Nếu HF dai dẳng mạn tính bị thoái hóa, bệnh nhân có thể được mô tả như là "mất bù" (decompensated) và điều này có thể xảy ra đột ngột hoặc từ từ, thường dẫn đến phải nhập viện, một sự kiện có tầm quan trọng đáng kể đến tiên lượng. HF khởi phát mới (new - onset: de novo) cũng có thể hiện cấp, ví dụ, như một hậu quả của nhồi máu cơ tim cấp tính (AMI), hoặc trong biểu hiện bán cấp (dần dần), ví dụ, ở những bệnh nhân có bệnh cơ tim giãn (DCM), những người thường xuyên có triệu chứng trong nhiều tuần hoặc nhiều tháng trước khi chẩn đoán trở nên rõ ràng. Mặc dù các triệu chứng và dấu hiệu của suy tim có thể giải quyết, các rối loạn chức năng tim tiềm ẩn có thể không và bệnh nhân vẫn có nguy cơ tái phát 'mất bù”.
Tuy nhiên, đôi khi, bệnh nhân có thể có suy tim do một vấn đề được giải quyết hoàn toàn (vị dụ, như viêm cơ tim do virus cấp tính, bệnh cơ tim takotsubo hoặc bệnh cơ tim do nhịp nhanh). Các bệnh nhân khác, đặc biệt là những người DCM 'vô căn', cũng có thể hiện sự hồi phục đáng kể hoặc thậm chí hoàn toàn chức năng LV tâm thu với điều trị hiện thời làm thay đổi bệnh [bao gồm ức chế men chuyển angiotensin (ACEI), beta-blocker, chất đối kháng thụ thể mineralocorticoid (MRA), Ivabradine và / hoặc CRT]. 'HF sung huyết' là một thuật ngữ đôi khi được sử dụng, có thể mô tả HF cấp tính hoặc mạn tính với bằng chứng về quá tải khối lượng. Nhiều hoặc tất cả những thuật ngữ này có thể được áp dụng một cách chính xác đối với các bệnh nhân tương tự tại thời điểm khác nhau, tùy thuộc vào giai đoạn của bệnh.
3.2.3 Thuật ngữ liên quan đến mức độ nặng của suy tim có triệu chứng(Terminology related to the symptomatic severity of heart failure)
Phân loại NYHA chức năng (Web Bảng 3.2) đã được sử dụng để mô tả mức độ nghiêm trọng của các triệu chứng và không chịu đựng được gắng sức. Tuy nhiên, mức độ nặng của triệu chứng tương quan không đầy đủ với nhiều số đo của chức năng LV; mặc dù có một mối quan hệ rõ ràng giữa mức độ nghiêm trọng của các triệu chứng và sự sống còn, bệnh nhân có triệu chứng nhẹ vẫn có thể có nguy cơ tăng lên cho nhập viện và tử vong. [8-10]
Đôi khi thuật ngữ 'HF tiến triển' được sử dụng để mô tả các bệnh nhân có triệu chứng nặng, mất bù tái phát và rối loạn chức năng tim nặng. [11] ACCF/AHA phân loại mô tả các giai đoạn phát triển HF dựa trên thay đổi cấu trúc và triệu chứng (Web Bảng 3.3). [12] Phân loại Killip có thể được sử dụng để mô tả mức độ nghiêm trọng của tình trạng bệnh nhân trong bối cảnh cấp tính sau nhồi máu cơ tim (xem phần 12). [13]
Căn nguyên của HF là đa dạng trong và giữa các khu vực trên thế giới. Không có hệ thống phân loại thực sự được đồng nhất cho các nguyên nhân gây suy tim, có nhiều chồng chéo giữa các chủng loại tiềm năng (Bảng 3.4). Nhiều bệnh nhân có vài bệnh lý khác nhau - tim mạch và không phải tim mạch khác nhau và không tim mạch - chúng kết hợp lại gây suy tim. Xác định các bệnh lý khác nhau này nên là một phần của tiến dần đền chẩn đoán, vì chúng có thể đem lại cơ hội điều trị cụ thể.
Nhiều bệnh nhân bị bệnh tim thiếu máu cục bộ và HF (IHD) có tiền sử nhồi máu cơ tim hoặc tái thông mạch máu. Tuy nhiên, chụp động mạch vành bình thường không loại trừ vết sẹo cơ tim (ví dụ bằng hình ảnh CMR) hoặc suy vi mạch vành khi bằng chứng khác cho IHD.
Trong thực hành lâm sàng, sự phân biệt rõ ràng giữa các bệnh cơ tim mắc phải và di truyền vẫn còn khó khăn. Trong hầu hết các bệnh nhân với chẩn đoán lâm sàng xác định HF, không có vai trò khẳng định cho các test di truyền được làm đại trà, nhưng tư vấn di truyền được khuyến cáo ở những bệnh nhân có bệnh cơ tim phì đại (HCM), 'vô căn' DCM hoặc bệnh cơ tim thất phải gây loạn nhịp (ARVC) (xem phần 5.10.1), kể từ khi các kết quả của các test này có thể có quan hệ mật thiết lâm sàng.
Trong 30 năm qua, những cải tiến trong phương pháp điều trị và thực hiện chúng đã được cải thiện sự sống còn và giảm tỷ lệ nhập viện ở bệnh nhân HFrEF, mặc dù kết quả thường vẫn không đạt yêu cầu. Các dữ liệu gần đây nhất của châu Âu (ESC-HF pilot study) chứng minh tần số tử suất gây ra do mọi nguyên nhân trong 12 tháng ở các bệnh nhân phải nhập viện và suy tim dai dẳng / cấp cứu đã giảm là 17% và 7%, tương ứng, và tần số nhập viện 12 tháng là 44% và 32%, tương ứng. [35] Ở những bệnh nhân suy tim (cả hai nhập viện và cấp cứu), hầu hết các trường hợp tử vong là do nguyên nhân tim mạch, tử vong chủ yếu là đột ngột và suy tim xấu đi. Tử suất do mọi nguyên nhân thường cao hơn ở HFrEF so với HFpEF. [35, 36] Nhập viện thường do nguyên nhân không tim mạch, đặc biệt ở những bệnh nhân HFpEF. Nhập viện vì nguyên nhân tim mạch không thay đổi từ năm 2000 đến 2010, trong khi những người có nguyên nhân không phải tim mạch tăng lên. [31]
3.4 Tiên lượng(Prognosis)
Ước tính tiên lượng cho bệnh tật, tàn phế và tử vong giúp các bệnh nhân, gia đình và các bác sĩ của họ quyết định loại thích hợp và thời gian các phương pháp điều trị (đặc biệt là các quyết định về sự chuyển tiếp nhanh chóng sang các liệu pháp tiên tiến) và hỗ trợ với kế hoạch của y tế và dịch vụ xã hội cũng như nguồn lực.
Nhiều dấu hiệu tiên lượng tử vong và / hoặc suy tim nhập viện đã được xác định ở những bệnh nhân suy tim (Web Bảng 3.5). Tuy nhiên, ứng dụng lâm sàng của chúng bị hạn chế và phân tầng nguy cơ chính xác trong HF vẫn còn nhiều thách thức.
Trong những thập kỷ gần đây, một số điểm nguy cơ tiên lượng đa biến đã được phát triển cho các quần thể khác nhau của bệnh nhân suy tim, [36-41] và một số có sẵn như các ứng dụng trực tuyến tương tác. Các điểm số nguy cơ đa biến có thể giúp dự đoán tử vong ở bệnh nhân suy tim, nhưng vẫn ít hữu ích để dự báo số ca HF nhập viện tiếp theo. [37, 38] Một tổng quan hệ thống kiểm tra 64 mô hình tiên lượng [37], cùng với một phân tích và nghiên cứu hồi gộp của 117 mô hình tiên lượng [38] cho thấy chỉ có một độ chính xác trung bình của các mô hình dự báo tỷ lệ tử vong, trong khi mô hình được thiết kế để dự đoán các thiết tiêu chí tử vong hỗn hợp hoặc nhập viện, hoặc chỉ nằm viện, có một khả năng phân biệt còn kém hơn.
8. Điều trị suy tim có giảm phân suất tống máu bằng dụng cụ không phẫu thuật.
Phần này cung cấp các khuyến cáo về việc sử dụng các ICD và CRT. Hiện nay, các bằng chứng được xem là không đủ để hỗ trợ các khuyến cáo hướng dẫn chuyên biệt cho các kỹ thuật điều trị khác, bao gồm liệu pháp kích hoạt phản xạ áp lực (baroreflex), [217] kích thích phế vị, [218] tạo nhịp cơ hoành [219, 220] và điều biến sự co bóp của tim; [221, 222] nghiên cứu tiếp theo cần được đòi hỏi. Thiết bị cấy để theo dõi loạn nhịp hoặc huyết động học được thảo luận ở phần khác.
8.1 Máy khử rung tim có thể cấy
Một tỷ lệ tử vong cao ở những bệnh nhân suy tim, đặc biệt là những người có triệu chứng nhẹ hơn, xảy ra đột ngột và bất ngờ. Nhiều người trong số này là do rối loạn điện, gồm loạn nhịp thất, nhịp tim chậm và vô tâm thu, mặc dù một số là do biến cố mạch vành, não hoặc động mạch chủ. Phương pháp điều trị để cải thiện hoặc làm chậm tiến triển của bệnh tim mạch sẽ giảm tỷ lệ hàng năm của đột tử, nhưng chúng có thể có ít ảnh hưởng đến nguy cơ suốt đời và sẽ không xử lý được các biến cố loạn nhịp khi chúng xảy ra. ICD có hiệu quả trong việc ngăn ngừa nhịp chậm và điều chỉnh rối loạn nhịp thất có khả năng gây tử vong. Một số thuốc chống loạn nhịp có thể làm giảm tần số của nhịp nhanh và đột tử, nhưng chúng không làm giảm tử suất toàn bộ và có thể còn tăng.
Khuyến cáo cấy ICD ở các BN suy tim (KC 1)
Khuyến cáo
|
Classa
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Levelb
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Refv
|
Dự phòng thứ phát
ICD được khuyến cáo làm giảm nguy cơ SD và tử suất do mọi nguyên nhân ở các BN đã được hồi phục từ VA gây bất ổn huyết động và hy vọng sống sót > 1 năm với trạng thái chức năng tốt.
|
I
|
A
|
223-226
|
Dự phòng nguyên phát
ICD được khuyến cáo làm giảm nguy cơ SD và tử suất do mọi nguyên nhân ở BN có HF triệu chứng (NYHA Class II-III) và LVEF ≤ 35% mặc dù ≥ 3 tháng OMT, miễn họ đang hy vọng sống sót lâu hơn đáng kể so với một năm với tình trạng chức năng tốt và họ có:
- IHD (ngoại trừ họ đã có MI trong 40 ngày trước- xem dưới)
- DCM
| |||
I
I
|
A
|
149, 156, 227
156, 157, 227
| |
B
| |||
Cấy ICD không được khuyến cáo trong phạm vi 40 ngày của MI khi cấy trong thời gian này không cải thiện tiên lượng.
|
III
|
A
|
158, 228
|
Điều trị ICD không khuyến cáo ở BN NYHA Class IV với triệu chứng nặng trơ với điều trị thuốc ngoại trừ họ là ứng viên cho CRT, dụng cụ hỗ trợ thất, hoặc ghép tim.
|
III
|
C
|
229, 233
|
BN cần được các bác sỹ chuyên khoa tim có kinh nghiệm đánh giá cần thận trước khi thay máy, do các mục tiêu điều chỉnh và sự cần thiết của bệnh nhân và cả trạng thái lâm sàng có thể đã thay đổi.
|
IIa
|
B
|
234, 238
|
ICD mặc ngoài có thể được xem xét cho BN HF có nguy cơ SCD trong giai đoạn giới hạn hoặc như bắc cầu cho thiết bị cấy.
|
IIb
|
C
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239, 241
|
CAD: bệnh động mạch vành. CRT: điều trị tái đồng bộ; DCM: bệnh cơ tim giãn; HF: suy tim; ICD: máy khử rung tim có thể cấy; IHD: bệnh tim thiếu máu cục bộ; LVEF: phân suất tống máu. MI: nhồi máu cơ tim. NYHA: New York Heart Association. OMT: điều trị thuốc tối ưu.
aClass khuyến cáo.
bMức độ bằng chứng.
cTài liệu tham khảo ủng hộ khuyến cáo.
|
8.1.1 Dự phòng đột tử tim thứ phát
So sánh với điều trị amiodarone, ICD làm giảm tử suất trong sống sót sau ngừng tim và ở các bệnh nhân đã trải qua loạn nhịp thất (VA) có triệu chứng dai dẳng. ICD được khuyến cáo ở các bệnh nhân như vậy khi mục đích làm tăng sống sót; quyết định cấy nên đưa vào tính toán toàn cảnh bệnh nhân và chất lượng đời sống của họ, LVEF (lợi ích sống còn là không chắc chắn khi LVEF > 35%) và sự vắng mặt của các bệnh khác có khả năng gây tử vong trong vòng một năm sau.[223-225]
8.1.2 Dự phòng đột tử tim nguyên phát
Mặc dù amiodarone có thể làm giảm tử suất trong các nghiên cứu HF trước,[242, 243] các nghiên cứu hiện thời được thực hiện từ khi hướng dẫn sử dụng rộng rãi beta blốcers gợi ý nó không làm giảm tử suất ở BN HFrEF.[227, 244, 245] Dronedarone [246, 247] và các thuốc chống loạn nhịp class I [246, 248] không nên sử dụng để dự phòng loạn nhịp ở quần thể bệnh nhân này.
Một số điều trị được hướng dẫn khuyến cáo, gồm beta-blockers, MRAs, sacubitril/valsartan và tạo nhịp với CRT (CRT-Ps), làm giảm nguy cơ đột tử.
ICD làm giảm tần số đột tử do loạn nhịp (SAD) ở các bệnh nhân HFrEF.[249, 250] Ở những bệnh nhân suy tim vừa hoặc nặng, giảm SD có thể được một phần hoặc hoàn toàn bù đắp bởi sự gia tăng tử vong do HF xấu đi. [227] Ở những bệnh nhân suy tim nhẹ (NYHA II), ICD sẽ ngăn chặn khoảng hai ca tử vong mỗi năm cho mỗi 100 thiết bị cấy. [227] Trung bình, bệnh nhân IHD có nguy cơ SD lớn hơn so với bệnh nhân DCM và do đó, mặc dù những lợi ích tương đối giống nhau, những lợi ích tuyệt đối là lớn hơn ở những bệnh nhân với IHD. [249] Bệnh nhân với thời gian QRS dài hơn cũng có thể nhận được lợi ích lớn hơn từ ICD, nhưng những bệnh nhân này thường sẽ nhận được CRT. [227, 251]
Hai RCTs cho thấy không có lợi ích ở bệnh nhân được cấy ICD trong phạm vi 40 ngày sau nhồi máu cơ tim.[158, 228] Mặc dù SAD có giảm, điều này được cân bằng bằng tăng tử vong do không phải loạn nhịp. Theo đó, ICD được chống chỉ định trong khoảng thời gian này. Một máy khử rung tim mặc ngoài có thể được xem xét nếu bệnh nhân được coi là có nguy cơ cao bị rung thất, mặc dù thiếu bằng chứng từ các thử nghiệm ngẫu nhiên. [239-241]
Cấy ICD được khuyến cáo chỉ sau trải nghiệm đầy đủ (tối thiểu 3 tháng) của điều trị nội khoa tối ưu (OMT) đã thất bại trong việc tăng LVEF đến > 35%. Tuy nhiên, một trong hai bài luận trình mang tính đánh dấu làm chứng trên đó các khuyến cáo này dựa trên bao gồm những bệnh nhân có LVEF> 30%. Ít hơn 400 bệnh nhân với một LVEF 30-35% được bao gồm trong các nghiên cứu đánh dấu làm chứng, mặc dù không có sự tương tác thống kê giữa hiệu quả điều trị và LVEF, các chứng cứ có lợi là ít mạnh mẽ ở nhóm bệnh nhân này.
Lập trình kinh điển với thời gian trễ kéo dài [252] giữa phát hiện và điều trị phóng điện của ICD làm giảm đáng kể nguy cơ của cả sốc không phù hợp (do nhận nhầm hoặc AF) và sốc phù hợp nhưng không cần thiết [do nhịp nhanh thất (VT) tự ngừng]. [252- 254]
Bệnh nhân có thời gian QRS ≥ 130 ms nên được xem xét cho máy khử rung tim với chức năng tái đồng bộ CRT (CRT-D) hơn là ICD. Xem các hướng dẫn cho CRT để biết thêm chi tiết. Điều trị ICD không được khuyến cáo ở những bệnh nhân trong NYHA class IV với các triệu chứng nghiêm trọng trơ với điều trị bằng thuốc không phải là ứng cử viên cho CRT, một thiết bị hỗ trợ tâm thất hoặc ghép tim, do các bệnh nhân này có tuổi thọ rất hạn chế và có thể chết vì suy bơm.
Bệnh nhân có bệnh nghiêm trọng, những người không có khả năng sống sót đáng kể hơn 1 năm, không có khả năng thu được lợi ích đáng kể từ một ICD. [229-233]
Bệnh nhân cần được tư vấn như mục đích của ICD, các biến chứng liên quan đến cấy và kích hoạt thiết bị (chủ yếu là không phù hợp) và trong hoàn cảnh nào nó có thể bị ngừng hoạt động (bệnh kết thúc) hoặc được lấy bỏ (nhiễm trùng, phục hồi chức năng LV). [255]
Nếu HF thoái biến, làm mất hoạt động của ICD của bệnh nhân có thể được xem xét sau khi thảo luận phù hợp với bệnh nhân và người chăm sóc.
Nếu máy ICD đến kết thúc của cuộc sống hay đòi hỏi lấy bỏ, không nên tự động thay. [234-238] Bệnh nhân cần được bác sỹ chuyên khoa tim mạch có kinh nghiệm đánh giá cẩn thận trước khi thay máy. Mục tiêu điều trị có thể đã thay đổi và nguy cơ loạn nhịp tim gây tử vong có thể thấp hơn hoặc nguy cơ tử vong không loạn nhịp cao hơn. Đó là vấn đề của một số tranh cãi cho dù bệnh nhân có LVEF đã cải thiện rất nhiều và những người đã không cần dùng liệu pháp thiết bị trong suốt thời gian hoạt động của ICD nên có một dụng cụ khác để cấy. [234-238]
Máy khử rung tim dưới da có thể hiệu quả như ICD thông thường với một nguy cơ thấp hơn so với quy trình cấy máy. [256, 257] Chúng có thể là lựa chọn ưa thích cho bệnh nhân đi lại khó khăn hoặc cần lấy ICD ra ngoài do nhiễm trùng. Bệnh nhân phải được lựa chọn cẩn thận, như họ đã hạn chế khả năng để điều trị rối loạn nhịp chậm nghiêm trọng và có thể đưa ra không phải tạo nhịp chống nhịp nhanh cũng không phải CRT. RCT có ý nghĩa với các thiết bị này và tư liệu nhiều hơn về tính an toàn và hiệu quả cần được chờ đợi. [258, 259]
ICD mặc (một máy khử rung tim bên ngoài với dây dẫn và miếng điện cực gắn liền với một chiếc áo khoác có thể mặc được) có thể phát hiện và cắt VT/VF có thể được xem xét trong khoảng hạn chế về thời gian ở những bệnh nhân được lựa chọn với HF, những người có nguy cơ cao bị SD, nhưng còn không thích hợp cho cấy ICD (ví dụ như những người có LVEF xấu sau khi tổn thương cơ tim cấp tính cho đến khi chức năng LV phục hồi, bệnh nhân lên kế hoạch cho việc ghép tim). [239-241, 260] Tuy nhiên, không có RCT tiền cứu đánh giá thiết bị này được báo cáo.
Cho các khuyến cáo chi tiết về sử dụng / chỉ định ICD người ta đề nghị độc giả đọc các hướng dẫn của ESC/EHRA (ESC/European Heart Rhythm Association: EHRA) về loạn nhịp thất và đột tử.[260] Chúng tôi đã đang một loạt trong các số của chuyên đề tim mạch các số trước đây.
8.2 Điều trị tái đồng bộ tim
Các khuyến cáo cho điều trị tái đồng bộ tim cho các bệnh nhân suy tim (KC 2)
Các khuyến cáo
|
Classa
|
Levelb
|
Refc
|
CRT được khuyến cáo cho các bệnh nhân HF có triệu chứng có nhịp xoang với khoảng QRS ≥ 150ms và hình thái QRS LBBB và với LVEF ≤ 35% mặc dù OMT để cải thiện triệu chứng và giảm bệnh suất và tử suất.
|
I
|
A
|
261, 272
|
CRT được khuyến cáo cho các bệnh nhân HF có triệu chứng nhịp xoang với khoảng QRS ≥ 150ms và không có hình thái QRS LBBB và với LVEF ≤ 35% mặc dù OMT để cải thiện triệu chứng và giảm bệnh suất và tử suất.
|
IIa
|
B
|
261, 272
|
CRT được khuyến cáo cho các bệnh nhân HF có triệu chứng nhịp xoang với khoảng QRS ≥ 130 – 149 ms và hình thái QRS LBBB và với LVEF ≤ 35% mặc dù OMT để cải thiện triệu chứng và giảm bệnh suất và tử suất.
|
I
|
B
|
266, 273
|
CRT được khuyến cáo cho các bệnh nhân HF có triệu chứng nhịp xoang với khoảng QRS ≥ 130 - 149ms và không có hình thái QRS LBBB và với LVEF ≤ 35% mặc dù OMT để cải thiện triệu chứng và giảm bệnh suất và tử suất.
|
IIb
|
B
|
266, 273
|
CRT hơn tạo nhịp thất phải được khuyến cáo cho các bệnh nhân HFrEF bất chấp class NYHA người có chỉ định tạo nhịp thất và blốc AV cao độ để giảm tử suất. Điều này gồm các bệnh nhân AF (xem phân 10.1)
|
I
|
A
|
274, 277
|
CRT cần được xem xét cho các bệnh nhân LVEF ≤ 35% với NYHA class III-IVdmặc dù OMT để cải thiện triệu chứng và giảm bệnh suất và tử suất, nếu họ có AF và khoảng thời gian QRS ≥ 130 ms được cung cấp chiến lược để đảm bảo đạt được hai thất được đặt ra hoặc các bệnh nhân mong đợi trở vể nhịp xoang.
|
IIa
|
B
|
275, 278, 281
|
Bệnh nhân HFrEF nhận được tạo nhịp thông thường hoặc ICD, tiếp theo phát triển HF xấu đi mặc dù OMT và họ có tỷ lệ cao tạo nhịp thất phải có thể xem xét nâng cấp lên CRT. Điều này không áp dụng với bệnh nhân HF ổn định.
|
IIb
|
B
|
282
|
CRT chống chỉ định ở bệnh nhân có khoảng thời gian QRS < 130 ms
|
III
|
A
|
266, 283, 285
|
AF: rung nhĩ; AV: nhĩ thất; CRT: điều trị tái đồng bộ tim; HF: suy tim; HFrEF: suy tim phân suất giảm; ICD: máy khử rung tim có thể cấy; LBBB: blốc nhánh bó trái; NYHA: New York Heart Association; OMT: điều trị thuốc tối ưu; QRS: các sóng Q, R và S (phức hợp của 3 độ lệch); RV: thất phải.
a Class khuyến cáo
bMức độ bằng chứng
cTài liệu tham khảo ủng hộ khuyến cáo
dSử dụng phán quyết cho các bệnh nhân HF giai đoạn cuối, họ có thể được điều chỉnh kinh điển hơn với điều trị để cải thiện triệu chứng hoặc tiên lượng.
|
CRT cải thiện hiệu suất tim ở những bệnh nhân được lựa chọn một cách thích hợp và cải thiện các triệu chứng [286] và phúc lợi [286] và làm giảm bệnh suất và tử suất. [266] Trong số những cải thiện tuổi thọ chất lượng sống được điều chỉnh (quality adjusted life years: QALYs) với CRT trong số bệnh nhân HF vừa đến nặng, hai phần ba có thể là do cải thiện chất lượng cuộc sống và một phần ba để tăng tuổi thọ. [287] Chỉ có nghiên cứu COMPANION [265] và CARE-HF [262, 263] so sánh ảnh hưởng của CRT với điều trị thuốc khuyến theo hướng dẫn. Hầu hết các nghiên cứu khác đã so sánh CRT-D đối với ICD, một vài người đã so sánh CRT-P để tạo nhịp dự phòng. Việc phòng ngừa nhịp chậm nguy hiểm có thể là một cơ chế quan trọng của lợi ích được chia sẻ do tất cả các thiết bị tạo nhịp. Trong CARE-HF, 25% bệnh nhân có nhịp tim lúc nghỉ ≤ 60 bpm. [262-264] Nếu dự phòng nhịp tim chậm là quan trọng, tác dụng của CRT sẽ xuất hiện nhiều hơn trong các thử nghiệm mà không có thiết bị trong nhóm đối chứng.
Hầu hết các nghiên cứu về CRT đã xác định LVEF nên < 35%, nhưng RAFT [267] và MADIT-CRT [268, 269] được ghi rõ LVEF < 30%, trong khi REVERSE [270-272] ghi rõ < 40% và BLỐC - HF [274] < 50%. Tương đối ít bệnh nhân với LVEF 35-40% đã được chọn ngẫu nhiên, nhưng phân tích gộp tư liệu tham giam mang tính cá thể gợi ý không có giảm về hiệu quả CRT trong nhóm này. [266]
Không phải tất cả các bệnh nhân đáp ứng thuận lợi với CRT. [286] Một số đặc điểm dự đoán cải thiện bệnh suất và tử suất, và mức độ tái cấu trúc hồi phục là một trong những cơ chế quan trọng nhất của hoạt động CRT. Bệnh nhân có nguyên nhân thiếu máu cục bộ sẽ có ít cải thiện chức năng LVdo mô sẹo cơ tim, các tổ chức cơ tim này ít có khả năng thực hiện tái cấu trúc thuận lợi. [288] Ngược lại, phụ nữ có thể có nhiều khả năng để đáp ứng nhiều hơn nam giới, có thể do cơ thể và kích thước tim nhỏ hơn. [273, 285, 289] QRS rộng dự đoán đáp ứng CRT và là tiêu chuẩn đưa vào tất cả các thử nghiệm ngẫu nhiên. Nhưng hình thái QRS cũng đã được liên quan đến đáp ứng có lợi cho CRT. Một số nghiên cứu đã chỉ ra bệnh nhân có hình thái blốc bó nhánh trái (LBBB) có nhiều khả năng để đáp ứng thuận lợi với CRT, trong khi có ít sự chắc chắn về những bệnh nhân không có hình thái LBBB. Tuy nhiên, bệnh nhân hình thái LBBB thường có thời gian QRS rộng hơn, có một cuộc tranh luận hiện nay về việc liệu thời gian QRS hoặc hình thái QRS là yếu tố dự báo chính của đáp ứng có lợi cho CRT hay không. Bằng chứng từ hai phân tích gộp IPD cho thấy sau khi tính toán cho thời gian QRS, có rất ít bằng chứng cho thấy hình thái QRS hoặc bệnh căn ảnh hưởng đến hiệu quả của CRT lên bệnh suất và tử suất. [266, 273] Ngoài ra, không có nghiên cứu đánh dấu so sánh các bệnh nhân được lựa chọn để đưa vào hình thái QRS, giới hoặc căn nguyên thiếu máu cục bộ, cũng không có những nghiên cứu đủ mạnh cho các phân tích phân nhóm.
Nghiên cứu Echo-CRT[283, 284] và phân tích gộp IPD [266] gợi ý có thể có hại do CRT khi khoảng thời gian QRS <130 ms, do đó cấy CRT không được khuyến cáo nếu khoảng thời gian QRS <130 ms.[266, 283, 284]
Nếu một bệnh nhân dự kiến sẽ nhận được ICD và đang nhịp xoang với khoảng thời gian QRS ≥130 ms, CRT-D nên được xem xét nếu QRS giữa 130 và 149 ms và được khuyến khích nếu QRS là ≥150 ms. Tuy nhiên, nếu những lý do chính cho cấy CRT là để làm giảm các triệu chứng, sau đó các bác sĩ lâm sàng nên chọn CRT-P hoặc CRT-D, cái nào họ cho là phù hợp. Thực hành lâm sàng rất khác nhau giữa các nước. Các thử nghiệm ngẫu nhiên chỉ để so sánh CRT-P và CRT-D [265] không cho thấy sự khác biệt trong bệnh suất và tử suất giữa các công nghệ này. [288] Nếu lý do chính cho việc cấy CRT là để cải thiện tiên lượng, sau đó phần lớn bằng chứng nằm ở CRT-D cho các bệnh nhân trong NYHA class II và với CRT-P cho bệnh nhân trong NYHA class III-IV. Hiện chưa rõ liệu CRT giảm sự cần thiết cho một ICD (bằng cách giảm gánh nặng rối loạn nhịp tim) hoặc làm tăng lợi ích từ ICD (bằng cách giảm tỷ lệ tử vong do HF xấu đi, dẫn đến bộc lộ lâu hơn đến nguy cơ rối loạn nhịp tim).
Khi LVEF giảm, tạo nhịp thất phải có thể làm trầm trọng thêm mất đồng bộ tim. Điều này có thể được ngăn ngừa bằng CRT, mà có thể cải thiện kết cục bệnh nhân. [274, 275, 277, 290] Tuy nhiên, một sự khác biệt trong kết quả đã không quan sát được giữa CRT và tạo nhịp RV trong một phân tích phân nhóm của RAFT [267] hoặc ở những bệnh nhân không có HFrEF trong BioPACE. [291] Sau khi cân nhắc, CRT hơn tạo nhịp RV được khuyến cáo cho bệnh nhân HFrEF bất kể class NYHA người có chỉ định cho nhịp tâm thất để giảm bệnh suất, mặc dù không có tác dụng rõ ràng về tỷ lệ tử vong đã được quan sát. Bệnh nhân HFrEF người đã nhận được một máy tạo nhịp tim thông thường hoặc một ICD và sau đó phát triển HF xấu đi với một tỷ lệ cao của tạo nhịp RV, mặc dù OMT, cần được xem xét nâng cấp lên CRT.
Chỉ có hai thử nghiệm nhỏ đã so sánh điều trị thuốc đơn thuần so với CRT ở bệnh nhân RN, với kết quả trái ngược. Một số nghiên cứu đã chỉ ra CRT ưu thế hơn tạo nhịp RV ở bệnh nhân trải qua triệt phá nút AV (AV). [275, 277, 290] Tuy nhiên, CRT không phải là một dấu hiệu để thực hiện triệt phá nút AV, ngoại trừ trong trường hợp hiếm hoi khi tỷ lệ thất vẫn nhanh dai dẳng (> 110 bpm) bất chấp các nỗ lực kiểm soát tần số bằng thuốc. Phân tích nhóm nhỏ bệnh nhân AF từ nghiên cứu RAFT không tìm thấy lợi ích từ CRT-D so với ICD, mặc dù ít hơn một nửa số bệnh nhân có > 90% tạo nhịp hai thất. [276] Nghiên cứu quan sát báo cáo tạo nhịp hai thất là < 98%, tiên lượng của bệnh nhân với CRT giảm. [277] Cho dù liên kết này phản ánh sự mất tái đồng bộ (có thể được khắc phục bằng cách lập trình thiết bị), đặt điện cực thất trái (LV) kém (mà có thể được tránh lúc cấy) hoặc gặp khó khăn hơn trong tạo nhịp cơ tim bị bệnh nặng (có thể không tuân theo như trên) là không chắc chắn. Quan sát này chưa được xác nhận trong một thử nghiệm ngẫu nhiên.
Test hình ảnh cho rối loạn đồng bộ (dyssynchrony) còn không nhận thấy giá trị ở các bệnh nhân lựa chọn cho CRT. [292] Những bệnh nhân có vết sẹo cơ tim lan rộng sẽ có ít cải thiện chức năng LVvới CRT, nhưng điều này đúng với bất kỳ điều trị cho HFrEF và không đáng tin cậy dự đoán lợi ích lâm sàng ít hơn. [293] Ngưỡng tạo nhịp cao hơn trong cơ tim đã thành sẹo, nếu có thể, vị trí đặt điện cực nên tránh các khu vực đó. [294, 295] Mặc dù bệnh nhân có sẹo lan rộng có một tiên lượng về thực chất xấu hơn, có rất ít bằng chứng cho thấy chúng có được lợi ích tiên lượng ít hơn từ CRT. [266]
Độc giả được hướng đến hướng dẫn về tạo nhịp và CRT cho các khuyến cáo về thủ thuật cấy thiết bị. Giá trị của nỗ lực để tối ưu hóa các khoảng AV hoặc VV sau cấy sử dụng các tiêu chuẩn siêu âm hoặc điện tâm đồ hoặc đáp ứng huyết áp là không chắc chắn, nhưng có thể được xem xét cho những bệnh nhân đã có một đáp ứng không mong đợi cho CRT. [296, 297]
8.3 Các thiết bị điện có thể cấy khác
Đối với bệnh nhân HFrEF vẫn còn có triệu chứng mặc dù OMT và không có chỉ định cho CRT, liệu pháp thiết bị mới đã được đề xuất và trong một số trường hợp được chấp thuận cho sử dụng lâm sàng ở một số nước Liên minh châu Âu (EU) nhưng vẫn còn được đánh giá thử nghiệm.
Điều biến co bóp tim (cardiac contractility modulation: CCM) cũng tương tự như trong chế độ của nó đưa vào cho CRT, nhưng nó liên quan đến sự kích thích điện không kích thích của tâm thất trong thời gian trơ tuyệt đối để nâng cao hiệu suất co mà không kích hoạt tâm thất thu thêm. CCM đã được đánh giá ở bệnh nhân HFrEF mức NYHA class II-III với QRS giới hạn bình thường (<120 ms). [221, 222] Một dữ liệu bệnh nhân phân tích gộp cá nhân đã chứng minh sự cải thiện khả năng dung nạp gắng sức (đỉnh VO2) và chất lượng cuộc sống (Bảng hỏi Cuộc sống Suy tim Minnesota: Minnesota Living with Heart Failure questionnaire). Như vậy CCM có thể được xem xét ở những bệnh nhân HF được lựa chọn. Hiệu quả của CCM về bệnh suất và tử suất do HF còn đang được xác lập.
Hầu hết các thiết bị khác được đánh giá liên quan đến một số sửa đổi các hoạt động của hệ thần tự động (autonomic nervous system: ANS) bằng cách kích thích điện có đích. [298, 299] Chúng bao gồm kích thích thần kinh phế vị, kích thích tủy sống, triệt phá thân carotid và bóc bỏ thần kinh thận, nhưng cho đến nay không có của các thiết bị nào cải thiện triệu chứng hoặc kết quả trong RCT.
Các thiết bị cho theo dõi từ xa được thảo luận riêng.
10. Rối loạn nhịp và rối loạn dẫn truyền
Theo dõi điện tâm đồ Ambulatory có thể được sử dụng để khảo sát các triệu chứng có thể là do loạn nhịp tim, [322-324] nhưng bằng chứng còn thiếu để hỗ trợ thường xuyên, theo dõi hệ thống cho tất cả các bệnh nhân suy tim để xác định rối loạn nhịp nhanh và nhịp chậm. Không có bằng chứng các quyết định lâm sàng dựa trên theo dõi điện tim lưu động thường xuyên cải thiện kết quả cho bệnh nhân HF.
Ghi điện tâm Ambulatory phát hiện phức hợp thất sớm ở hầu như tất cả các bệnh nhân suy tim. Các cơn VT có triệu chứng, tạm thời là phổ biến, ngày càng tăng ở tần số với mức độ nặng của suy tim và rối loạn chức năng tâm thất và chỉ ra một tiên lượng xấu cho bệnh nhân HF, nhưng cung cấp ít sự phân biệt giữa SD howc tử vong do HF tiến triển. [316, 325 ] Nhịp tim chậm và các khoảng ngưng cũng thường được quan sát, đặc biệt vào ban đêm khi hoạt động giao cảm thường thấp và hoạt động kinh đối giao cảm cao hơn; ngưng thở khi ngủ có thể là một khởi kích. [326-328] Các đoạn ngưng được liên kết với một tiên lượng xấu của bệnh nhân CAD và rối loạn chức năng thất trái. [329] Rối loạn nhịp chậm có thể góp phần quan trọng đối với SD trong HF. [330]
10.1 Rung nhĩ (AF)
AF là rối loạn nhịp tim phổ biến nhất trong HF không phân biệt LVEF kèm theo; nó làm tăng nguy cơ biến chứng huyết khối tắc mạch (đặc biệt là đột quỵ) và có thể làm giảm chức năng tim, làm xấu đi triệu chứng HF. [316] HF phụ thuộc được thúc đẩy bằng AF được kết hợp với tiên lượng lành tính hơn, [331] nhưng khởi phát AF mới ở bệnh nhân với HF được tính toán được kết hợp với hậu quả xấu hơn, có lẽ vì do cả hai chỉ dấu bệnh nhân bệnh hơn và do làm suy yếu chức năng tim. [332, 333] Bệnh nhân suy tim mạn tính và AF vĩnh viễn có một kết quả xấu hơn so với các bệnh nhân nhịp xoang , mặc dù điều này phần lớn được giải thích do tuổi cao hơn và HF mức độ nghiêm trọng. [332, 333] Tần số thất dai dẳng > 150 bpm có thể gây HFrEF điều này mất đi bằng kiểm soát tần số hoặc sửa chữa nhịp ( 'bệnh cơ tim do nhịp nhanh'). [334, 335] AF cần phân loại và điều chỉnh theo hướng dẫn AF hiện thời (tức cơn đầu tiên được chẩn đoán, kịch phát, dai dẳng, dai dẳng kéo dài hoặc vĩnh viễn), nhận biết không chắc chắn về thời gian thực sự của cơn và về các cơn không được phát hiện trước đó. [316]
Các vấn đề tiếp theo cần được xem xét ở những bệnh nhân suy tim có biểu hiện AF, không phân biệt LVEF, đặc biệt với cơn được chẩn đoán đầu tiên của AF hoặc AF kịch phát: [316] xác định nguyên nhân có khả năng sửa chữa được (ví dụ như suy giáp hoặc cường giáp, rối loạn điện giải, tăng huyết áp không kiểm soát được , bệnh van hai lá) và các yếu tố thúc đẩy (ví dụ như phẫu thuật gần đây, nhiễm trùng ngực hoặc đợt cấp của COPD / hen phế quản, thiếu máu cơ tim cấp, uống rượu say), vì điều này có thể xác định chiến lược điều chỉnh; đánh giá nguy cơ đột quỵ và cần cho thuốc chống đông máu; đánh giá tần số thất và nhu cầu kiểm soát tần số; đánh giá các triệu chứng của suy tim và AF.
Để biết chi tiết, đọc giả nên tham khảo hướng dẫn ESC về AF năm 2016. [316]
10.1.1 Ngăn ngừa rung nhĩ ở các bệnh nhân suy tim
Nhiều điều trị suy tim, gồm ACEIs, [336] ARB, [337] beta blockers [177, 338] và MRA, [339, 340] sẽ làm giảm tỷ lệ AF, nhưng Ivabradine có thể làm tăng. [341] CRT có ít ảnh hưởng đến tỷ lệ AF. [342]
Amiodaron sẽ làm giảm tỷ lệ AF, tạo ra chuyển nhịp bằng thuốc, duy trì nhiều bệnh nhân ở nhịp xoang sau khi chuyển nhịp và có thể được sử dụng để kiểm soát các triệu chứng ở những bệnh nhân AF kịch phát nếu beta-blockers thất bại. [343-346] Amiodarone nói chung nên được giới hạn sử dụng ngắn hạn (< 6 tháng) ở những bệnh nhân AF kịch phát hoặc AF dai dẳng để giúp đạt được nhịp xoang và giảm tỷ lệ cao của AF tái phát ngay lập tức sau khi chuyển nhịp. Dronedaron chống chỉ định ở bệnh nhân suy tim và AF. [246, 247, 347]
10.1.2 Điều chỉnh rung nhĩ khởi phát mới, rung nhĩ nhanh ở bệnh nhân suy tim
Nếu bệnh nhân không có triệu chứng lo lắng do HF, khi đó điều trị bằng uống beta blốcers có thể được bắt đầu để cung cấp kiểm soát tần số thất. Đối với bệnh nhân bị xung huyết đáng kể những người dù sao có vài triệu chứng khi nghỉ, điều trị ban đầu với đường uống hoặc tiêm tĩnh mạch (i.v.) digoxin được ưa thích. Đối với bệnh nhân đang huyết động không ổn định, bolus tĩnh mạch digoxin hoặc amiodarone [348, 349] nên được dùng đường tĩnh mạch rất cẩn thận để tránh thoát mạch vào mô; nơi không chắc chắn có tĩnh mạch để truyền, amiodarone không được cho. Truyền kéo dài amiodarone nên được sử dụng chỉ ở tĩnh mạch trung tâm hoặc tĩnh mạch lớn để tránh viêm tĩnh mạch ngoại vi. Ở những bệnh nhân huyết động suy sụp, cần chuyển nhịp bằng điện khẩn cấp được khuyến cáo (xem thêm Phần 12).
Khuyến cáo cho điều chỉnh khởi đầu của tần số thất nhanh ở các bệnh nhân HF và AF trong tình huống cấp và mạn tính (KC 3)
Khuyến cáo
|
Classa
|
Levelb
|
Refc
|
Chuyển nhịp bằng điện khẩn cấp được khuyến cáo nếu AF được cho là đã thúc đẩy tổn thương huyết động của bệnh nhân để cải thiện trạng thái lâm sàng của bệnh nhân
|
I
|
C
| |
Đối với BN NYHA Class IV trong điều kiện điều trị AHF bolus tĩnh mạch amiodarone hoặc, ở những BN trước đây chưa dùng digoxin, bolus tĩnh mạch digoxin nên được xem xét để giảm tần số thất.
|
IIa
|
B
|
348, 349
|
Đối với BN NYHA Class I-III, beta blốcer thường cho uống, an toàn cho nên được khuyến cáo như một điều trị lựa chọn đầu tiên để kiểm soát tần số thất,được cho bệnh nhân có thể tích phù hợp (euvolaemic)
|
I
|
A
|
177
|
Đối với BN NYHA Class I-III, digoxin, nên được xem xét khi tần số thất còn caod, mặc dù beta blốcer hoặc khi không dung nạp với beta blốcers hoặc có chống chỉ định.
|
IIa
|
B
|
197
|
Triệt phá nút AV có thể được xem xét để kiểm soát tần số tim và giảm bớt triệu chứng ở BN không đáp ứng hoặc không dung nạp với điều trị tần số thuốc mạnh hoặc kiểm soát nhịp, chấp nhận những bệnh nhân này sẽ trở nên phụ thuộc vào máy tạo nhịp.
|
IIb
|
B
|
290
|
Điều trị dronedarone không được khuyến cáo để cải thiện kiểm soát tần số thất do mối quan tâm (concerns) về an toàn
|
III
|
A
|
347
|
AF: rung nhĩ; AHF: suy tim cấp; AV: nhĩ thất; bpm: chu kỳ trên phút; HF: suy tim; NYHA: New York Heart Association.
aClass khuyến cáo
b Mức độ bằng chứng.
c Tài liệu tham khảo ủng hộ cho khuyến cáo.
d Tần số thất tối ưu cho BB có HF và AF không được tính toán, nhưng bằng chứng chiếm ưu thế (prevailing) gợi ý kiểm soát tần số chặt chẽ (strict) có thể có hại (deleterious). Tần số thất lúc nghỉ ở phạm vi 60 đến 100 bpm có thể được xem xét trên cơ sở lựa chọn mới đây của Ban Đặc nhiệm, mặc dù một nghiên cứu gợi ý tần số thất lúc nghỉ trên 110 bpm có thể còn được chấp nhận, và điều này được khuyến cáo hiện thời do Hướng dẫn ESC vể AF. Điều này có thể được thử nghiệm và được tinh luyện bằng các nghiên cứu tiếp theo.
|
10.1.3 Kiểm soát tần số (Rate control)
Đánh giá kiểm soát tần số thất từ mạch quay là không lý tưởng, đặc biệt là ở những bệnh nhân suy tim, khi hoạt động thất có thể không thương xuyên tạo ra xung có thể sờ thấy (palpable). Kiếm soát tần số nên được chứng minh bằng ECG. Một thiết bị có thể mặc cho phép đánh giá được tần số thất lúc nghỉ, gắng sức và ngủ, nhưng giá trị của theo dõi thường xuyên vẫn chưa được tính toán. Thiết bị có thể cấy như máy tạo nhịp, CRT hoặc ICD cũng có thể được sử dụng để đo tần số thất.
Tần số thất tối ưu lúc nghỉ ở bệnh nhân AF và HF là không chắc chắn nhưng có thể từ 60-100 bpm. [350, 352-354] Một thử nghiệm cho thấy tần số thất lúc nghỉ lên đến 110 bpm vẫn có thể chấp nhận được, [198, 202] và năm 2016 hướng dẫn ESC cho AF năm 2016 khuyên ngưỡng này là mục tiêu điều trị kiểm soát tần số. [316] Tuy nhiên, Ban Đặc nhiệm tin rằng tần số thấp hơn cho bệnh nhân suy tim có thể thích hợp hơn (60-100 bpm). Tần số thất < 70 bpm được liên kết với kết quả xấu hơn. [351] Điều này có thể giải thích lý do tại sao beta-blockers tăng liều đến liều mục tiêu hướng dẫn không làm giảm tỷ lệ mắc bệnh hoặc tử vong ở bệnh nhân HFrEF và AF, [177] và cũng có thể giải thích sự liên kết giữa digoxin và kết cục xấu được báo cáo trong một số nghiên cứu quan sát của AF. [355-357] Tần số thất tối ưu trong khi gắng sức cũng chưa chắc chắn, nhưng có thể là <110 bpm khi tập thể dục nhẹ. [354] Beta-blockers, digoxin và sự kết hợp của chúng có thể được sử dụng để kiểm soát tần số thất. [358] Điều này không chắc chắn đó là cách tiếp cận tối ưu, nhưng beta-blockers xuất hiện an toàn như các thuốc lựa chọn đầu tiên, ngay cả khi nó không phải là rõ ràng chúng giảm bệnh suất và tử suất ở bệnh nhân AF. Beta-blockers làm giảm tần số thất trong thời gian hoạt động, trong khi digoxin gây ảnh hưởng lớn hơn vào ban đêm. [358] Tần số thất cao dai dẳng có thể chỉ ra nhiễm độc giáp hoặc hoạt động giao cảm quá mức do ứ huyết, điều này có thể đáp ứng với lợi tiểu. Mặc dù amiodarone và các chẹn canxi không dihydropyridin có thể làm giảm tần số thất, chúng có tác động bất lợi nhiều hơn và nói chung là nên tránh ở bệnh nhân HFrEF, cả với ít sự chắc chắn, ở những bệnh nhân với HFpEF và HFmrEF. Hiếm khi, tần số thất không thể giảm dưới 100-110 bpm bằng biện pháp thuốc đơn thuần và triệt phá nút nhĩ qua catheter với tạo nhịp tâm thất có thể được xem xét; trong tình huống này, đối với bệnh nhân HFrEF, CRT cần được xem xét thay vì tạo nhịp RV thông thường. Có rất ít bằng chứng, trừ từ nghiên cứu đăng ký, để hỗ trợ một chiến lược triệt phá nút AV và CRT so với điều trị bằng thuốc đơn thuần ở bệnh nhân AF và tần số thất lúc nghỉ <100-110 bpm (xem Phần 8.2). [281] Tuy nhiên, ở bệnh nhân có nhịp thất nhanh và các triệu chứng khó điều chỉnh, triệt phá nút AV có thể được xem xét. Ngoài ra, nếu bệnh nhân được chỉ định ICD, triệt phá nút AV với cấy CRT-D có thể là một lựa chọn ưa thích, đặc biệt là nếu bệnh nhân có triệu chứng vừa phải đến nặng.
10.1.4 Kiểm soát nhịp (Rhythm control)
Ở các bệnh nhân HF mạn tính, chiến lược kiểm soát nhịp (bao gồm cả chuyển nhịp bằng thuốc và điện) đã không được chứng minh là tốt hơn các chiến lược kiểm soát tần số trong việc giảm bệnh suất và tử suất. [359] Chuyển nhịp khẩn cấp được chỉ định chỉ khi AF được đe dọa tính mạng, nếu không cả hai HF và tần số thất nên được kiểm soát trước khi chuyển nhịp bằng sốc điện. Một chiến lược kiểm soát nhịp có lẽ là tốt nhất dành cho bệnh nhân với một nguyên nhân thứ phát gây AF có thể đảo ngược (ví dụ cường giáp) hoặc một yếu tố thúc đẩy rõ ràng (ví dụ viêm phổi gần đây) và ở những bệnh nhân có các triệu chứng khó chịu do AF sau khi tối ưu hóa kiểm soát tần số và điều trị suy tim. Việc sử dụng các thuốc chống loạn nhịp class I và dronedarone làm tăng bệnh suất và tử suất ở các bệnh nhân HF và AF cần tránh. [246, 247, 347] Amiodarone sẽ tạo ra một số bệnh nhân rung nhĩ mạn tính trở lại nhịp xoang, có thể làm giảm các cơn AF có triệu chứng và sẽ giúp duy trì bệnh nhân nhịp xoang sau khi chuyển nhịp tự phát hoặc chuyển nhịp bằng điện. [343-346] Khi sử dụng, nhu cầu tiếp tục uống amiodarone nên được thường xuyên xem xét và điều chỉnh.
Sự an toàn và hiệu quả của triệt phá qua catheter trong tâm nhĩ và tĩnh mạch phổi (PV) như là một chiến lược kiểm soát nhịp trong HF hiện tại không chắc chắn trừ bệnh cơ tim do nhip nhanh gây ra. [316] Một nghiên cứu nhỏ cho thấy triệt phá AF vượt trội so với triệt phá nút AV và CRT. [360] Một nghiên cứu khác, trong đó có 203 bệnh nhân AF dai dẳng, HF và thiết bị ICD hoặc CRT, cho thấy triệt phá AF vượt trội so với amiodarone trong việc điều chỉnh AF, điều này đã được liên kết với nhập viện do HF ít hơn và tử suất thấp hơn. Hai nghiên cứu nhỏ triệt phá AF so với kiểm soát tần số gặp nhiều thành công hỗn hợp cùng với các biến chứng thủ thuật và thành công trong cải thiện triệu chứng. [278, 279] Các bằng chứng gần đây nhất từ một phân tích gộp gồm 914 bệnh nhân cho thấy tỷ lệ thành công đáng khích lệ của triệt phá PV của AF ở bệnh nhân có rối loạn chức năng LV, với những cải thiện trong LVEF và dự trữ chức năng. [361] các kết quả này cần được khẳng định trong RCT liên tục như CASTLE AF, [362] AMICA và CABANA.
Khuyến cáo cho chiến lược kiểm soát nhịp ở các BN AF, HF có triệu chứng (NYHA Class II–IV) và rối loạn chức năng tâm thu thất trái và không có bằng chứng mất bù cấp (KC 4)
Khuyến cáo
|
Classa
|
Levelb
|
Refc
|
Chuyển nhịp bằng điện hoặc bằng thuốc với amiodarone có thể được xem xét ở BN có triệu chứng dai dẳng và hoặc dấu hiệu HF mặc dù OMT và kiểm soát tần số thất phù hợp để cải thiện trạng thái hoặc triệu chứng lâm sàng.
|
IIb
|
B
|
344
|
Triệt phá AF có thể được xem xét để phục hồi nhịp xoang cải thiện triệu chứng ở BN triệu chứng dai dẳng và hoặc dấu hiệu HF, mặc dù OMP và kiểm soát tần số thất phù hợp để cải thiện trạng thái hoặc triệu chứng lâm sàng.
|
IIb
|
B
|
279, 363
|
Amiodarone được có thể xem xét trước (và sau) chuyển nhịp bằng điện thành công để duy trì nhịp xoang.
|
IIb
|
B
|
342, 360
|
Dronedarone không được khuyến cáo do nguy cơ nhập viện tăng lên cho các nguyên nhân tim mạch và nguy cơ tử vong sớm tăng lên ở các BN NYHA Class III-IV.
|
III
|
A
|
247. 347
|
Các thuốc chống loạn nhịp class I không được khuyến cáo do nguy cơ tử vong sớm tăng lên.
|
III
|
A
|
248, 364, 365
|
AF: rung nhĩ; AHF: suy tim cấp; AV: nhĩ thất; bpm: chu kỳ trên phút; HF: suy tim; NYHA: New York Heart Association.
aClass khuyến cáo
b Mức độ bằng chứng.
c Tài liệu tham khảo ủng hộ cho khuyến cáo.
|
10.1.5 Dự phòng thuyến tắc
Bệnh nhân HF và AF nói chung nên được chống đông và cân bằng lợi ích và nguy cơ chảy máu (dùng thang điểm CHA2DS2-VASC và HAS-Bled;. Để biết chi tiết, xin vui lòng xem Bảng Web 10.1 và 10.2) nên được đánh giá theo khuyến cáo trong hướng dẫn của ESC cho AF. [316] Tỷ lệ đáng kể bệnh nhân HF sẽ có cả lợi ích và nguy cơ điểm ≥3, chỉ ra việc xem xét cẩn thận nên được đưa ra trước khi kê đơn thuốc chống đông đường uống và theo dõi thường xuyên sau đó là cần thiết (và các yếu tố nguy cơ chảy máu có thể sửa chữa được nhấn mạnh) nếu một thuốc chống đông đường uống được cho.
NOACs được ưa thích cho bệnh nhân suy tim có AF không có bệnh van tim, khi NOACs được so sánh với thuốc kháng vitamin K dường như ít nhất hiệu quả tương tự và thậm chí an toàn hơn (ít xuất huyết nội sọ) ở những bệnh nhân suy tim so với những người không có HF, [316, 366, 367] mặc dù mối quan tâm hiện hữu về sự an toàn của chúng ở những bệnh nhân lớn tuổi bị suy tim và chức năng thận kém [368, 369] [cho một mô tả chi tiết về sự tương tác giữa NOAC và chức năng thận, xem Heidbuchel et al. [370]]. Ở những bệnh nhân suy tim và AF người có van tim cơ học hoặc ít nhất có hẹp van hai lá trung bìn, chỉ uống kháng vitamin K nên được sử dụng để phòng ngừa đột quỵ huyết khối tắc mạch. [370]
Liều dabigatran nên được giảm xuống còn 110 mg b.i.d. khi thanh thải creatinin là 30-49 ml / phút, rivaroxaban đến 15 mg mỗi ngày và edoxaban tới 30 mg mỗi ngày khi độ thanh thải creatinin là 30-50 ml / phút và apixaban đến 2,5 mg hai lần mỗi ngày nếu bệnh nhân có hai hoặc nhiều vấn đề sau đây: ≥80 tuổi, creatinin huyết thanh ≥1.5 mg / dL hoặc trọng lượng cơ thể ≤60 kg. [370-375] Tóm tắt các khuyến cáo đối với công tác phòng chống huyết khối tắc mạch ở bệnh nhân suy tim có triệu chứng và AF kịch phát hoặc dai dẳng thường được thể hiện trong bảng khuyến cáo. Để biết thêm chi tiết, xin vui lòng tham khảo các hướng dẫn ESC gần đây về AF. [316]
Thiết bị làm tắc nhĩ trái có thể được xem xét ở bệnh nhân AF như thay thế cho thuốc chống đông đường uống người có nguy cơ cao cả thuyên tắc huyết khối và chảy máu để tránh nguy cơ xuất huyết do nguy cơ thuốc chống đông máu. [381, 382]
Khuyến cáo ngăn ngừa huyết khối thuyên tắc ở các bệnh nhân suy tim có triệu chứng (NYHA Class II-IV) và rung nhĩ cơn hoặc dai dẳng / mạn tính. (KC 5)
Khuyến cáo
|
Classa
|
Levelb
|
Refc
|
Thang điểm CHA2DS2-VASC VÀ HAS-BLED là công cụ được khuyến cáo ở các BN HF để tính toán nguy cơ huyết khối và nguy cơ chảy máu kết hợp với kháng đông, theo thứ tự.
|
I
|
B
|
376, 377
|
Kháng đông uống được khuyến cáo để dự phòng thuyên tắc huyết khối cho tất cả các BN có AF cơn hoặc dai dẳng và thang điểm CHA2DS2-VASC ≥ 2, không có chống chỉ định và bất kể chiến lược điều chỉnh nhịp hay tần số được sử dụng (gồm cả sau chuyển nhịp thành công)
|
I
|
A
|
372, 375, 378, 379
|
Điều trị NOAC chống chỉ định ở BN van cơ học hoặc ít nhất hẹp van 2 lá trung bình.
|
III
|
B
|
380
|
Ở bệnh nhân AF khoảng thời gian ≥48 h, hoặc khi khoảng thời gian của AF là không rõ, thuốc chống đông đường uống được khuyến cáo ở liều điều trị cho ≥3 tuần trước khi chuyển nhịp bằng sốc điện hoặc thuốc.
|
I
|
B
| |
Heparin tĩnh mạch hoặc LMWH và TOE chiến lược đã được hướng dẫn được khuyến cáo cho các bệnh nhân người đã không được điều trị với liều kháng đông trong ≥3 tuần và đòi hỏi chuyển nhịp bằng sốc điện hoặc thuốc cấp thiết cho một loạn nhịp đe dọa tính mạng.
|
I
|
C
| |
Sự kết hợp của thuốc chống đông đường uống và thuốc kháng tiểu cầu không được khuyến cáo ở những bệnh nhân bệnh mạch vành mãn tính (> 12 tháng sau một sự kiện cấp tính) hay bệnh động mạch khác, vì có nguy cơ cao bị chảy máu nghiêm trọng. Điều trị duy nhất với một kháng đông uống được ưa thích sau 12 tháng.
|
III
|
C
| |
Đối với bệnh nhân suy tim và AF không do van tim đủ điều kiện cho thuốc chống đông dựa trên một số điểm CHA2DS2-VASC, NOACs hơn warfarin cần được xem xét cho thuốc chống đông như NOACs có liên quan với giảm nguy cơ đột quỵ, xuất huyết nội sọ và tỷ lệ tử vong, trong đó lớn hơn những nguy cơ xuất huyết tiêu hóa.
|
IIa
|
B
|
367
|
AF: rung nhĩ; AHF: suy tim cấp; AV: nhĩ thất; bpm: chu kỳ trên phút; HF: suy tim; NYHA: New York Heart Association.
aClass khuyến cáo
b Mức độ bằng chứng.
c Tài liệu tham khảo ủng hộ cho khuyến cáo.
|
10.2 Rối loạn nhịp thất
Điều chỉnh rối loạn nhịp thất không triệu chứng khởi đầu gồm sửa chữa các bất thường điện giải, đặc biệt kali và magiê huyết thanh thấp, ngừng các tác nhân có thể gây loạn nhịp và, ở những bệnh nhân với HFrEF, tối ưu hóa điều trị bằng thuốc với ACEIs, beta-blockers, MRA và sacubitril / valsartan, tất cả đều làm giảm nguy cơ đột tử. [174, 177, 383, 384]
Sự liên quan lâm sàng của thiếu máu cục bộ cơ tim cho sự thúc đẩy loạn nhịp thất là không chắc chắn, mặc dù các trường hợp có thể rối loạn nhịp được tạo nên do thiếu máu cục bộ vẫn tồn tại. Thử nghiệm ngẫu nhiên tái thông mạch máu cho bệnh nhân HFrEF không làm giảm tỷ lệ tử vong chung, [107, 385] ngay cả trong các phân nhóm bệnh nhân bị đau thắt ngực hoặc thiếu máu cục bộ cơ tim, [115, 386] nhưng phân tích sâu hơn đã cho thấy một sự giảm đột tử. [387]
Amiodarone (thường kết hợp với một beta-blocker) có thể được sử dụng để ngăn chặn loạn nhịp thất có triệu chứng, nhưng nó có thể ảnh hưởng xấu đến tiên lượng, đặc biệt là ở những bệnh nhân suy tim nặng hơn. [227, 244] Các thuốc chống loạn nhịp khác nên `tránh. [247] Thay đổi (mdification) nền gây ra loạn nhịp bằng tần số radio qua catheter có thể giảm một số các sốc điện phù hợp của ICD và có thể được sử dụng để cắt các cơn bão loạn nhịp ở bệnh nhân HF và nhịp nhanh thất tái phát thường xuyên và do đó cần xem xét ở các bệnh nhân như vậy. Tìm kiếm sự tư vấn của các thành viên của Đội HF có chuyên môn về điện sinh lý được khuyến cáo ở những bệnh nhân có rối loạn nhịp thất khó kiểm soát. Để biết thêm chi tiết, chúng tôi mời độc giả xem các hướng dẫn ESC/EHRA về rối loạn nhịp thất và đột tử do tim. [260]
Bảng khuyến cáo điều chỉnh rối loạn nhịp trong suy tim (KC 6)
Các khuyến cáo
|
Classa
|
Levelb
|
Refc
|
Các yếu tố tăng nặng/thúc đẩy tiềm tằng (như kali, magiê huyết thành thấp, thiếu máu cục bộ tiếp diễn) cần phải tìm kiếm và sửa chữa ở các bệnh nhân rối loạn nhịp thất
|
IIa
|
C
| |
Điều trị beta blockers, MRA và saccubitril/valsartan làm giảm đột tử ở các bệnh nhân HFrEF và rối loạn nhịp thất (như cho các bệnh nhân khác) (xem chương 7)
|
I
|
A
|
162. 170, 175
|
Cấy ICD và CRT được khuyến cáo cho các bệnh nhân đã được lựa chọn với HFrEF (xem chương 8)
|
I
|
A
|
223, 226, 388
|
Một vài chiến lược được xem xét để làm giảm loạn nhịp tái phát có triệu chứng ở những bệnh nhân có ICD (hoặc ở bệnh nhân không thích hợp (eligible) cho ICD. Bao gồm chú ý các yếu tố nguy cơ và điều trị HF bằng thuốc tối ưu, amiodarone, triệt phá qua catheter và CRT.
|
IIa
|
C
| |
Sử dụng các thuốc chống loạn nhịp phổ biến không được khuyến cáo ở các bệnh nhân HF và rối loạn nhịp thất không triệu chứng do lo ngại về tính an toàn (HF xấu đi, thúc đẩy loạn nhịp và tử vong)
|
III
|
A
|
256. 248, 264, 265
|
ACEI: ức chế men chuyển; ARB: ức chế thụ cảm thể angiotensin; CRT: điều trị tái đồng bộ tim; CRT-D: điều trị khử rung tim tái đồng bộ: HF: suy tim; HFrEF: suy tim phân suât giảm. ICD: khử rung tim có thể cấy: MRA: kháng thụ thể mineralocorticoid.
|
10.3 Nhịp chậm có triệu chứng, các khoảng ngưng và blốc nhĩ thất
Hướng dẫn ESC về tạo nhịp và CRT được khuyến cáo can thiệp khi các khoảng ngừng vượt 6 s, thậm chí khi điều này không kết hợp với các triệu chứng. [389] Tuy nhiên, các khuyến cáo này đã được tạo ra chủ yếu cho bệnh nhân không có rối loạn chức năng cơ tim rõ ràng, và khoảng ngừng ngắn hơn có thể yêu cầu sự can thiệp ở bệnh nhân HFrEF. [329] Nếu khoảng ngưng > 3 s được xác định trên theo dõi điện tâm đồ, các thuốc nên được xem xét và các thuốc sau được ngừng hoặc giảm liều, bắt đầu với CCB hạn chế tỷ lệ sau đó amiodarone, digoxin và Ivabradine. Đối với bệnh nhân AF, giảm liều chẹn beta cho phép tỷ lệ thất nghỉ ngơi vào ban ngày sẽ tăng lên 70-90 bpm có thể được xem xét, vì bằng chứng cho thấy beta-blockers cải thiện kết cục ở bệnh nhân RN còn thiếu. [177] Đối với bệnh nhân có các khoảng ngừng nhưng vẫn nhịp xoang, giảm liều chẹn beta nên tránh trừ khi khoảng ngưng có triệu chứng, kéo dài hoặc thường xuyên, trong trường hợp giá trị tương đối của giảm liều, ngừng beta-blocker và tạo nhịp hai thất (biventricular) có thể được xem xét. Tuy nhiên, bằng chứng còn thiếu để hỗ trợ chiến lược tạo nhịp chỉ cho phép khởi đầu hoặc chuẩn liều điều trị chẹn beta trong khi không có chỉ định tạo nhịp kinh điển; chiến lược này không được khuyến cáo. Đối với bệnh nhân HFrEF và blốc AV-độ cao, CRT được ưa thích hơn tạo nhịp RV (mục 8.2). Khi nguyên nhân của nhịp tim chậm hoặc ngưng là bệnh nút xoang với dẫn truyền AV còn nguyên vẹn, các chiến lược điều trị sau đó tránh gây gây mất đồng bộ thất được ưa thích, mặc dù bằng chứng thử nghiệm lâm sàng để hỗ trợ ý kiến chuyên gia này cho bệnh nhân suy tim đang còn ít. Đối với chỉ định tạo nhịp khác, xin vui lòng tham khảo Hướng dẫn ESC trên nhịp và CRT. [389]
Khuyến cáo điều trị nhịp chậm trong suy tim (KC 7)
Các khuyến cáo
|
Classa
|
Levelb
|
Refc
|
Khi các khoảng ngưng > 3s được nhận thấy trên ECG, hoặc khi nhịp chậm có triệu chứng và tần số thất lúc nghỉ < 50c/p ở nhịp xoang hoặc < 60c/p khi AF, điều đó nên xem xét có cần kê thuốc để hạn chế tần số hay không: đối với bệnh nhân ở nhịp xoang, thuốc ức chế beta nên được giảm liều hoặc ngừng chỉ khi xấu đi
|
IIa
|
C
| |
Đối với bệnh nhân ngưng kéo dài hoặc thường xuyên có triệu chứng mặc dù điều chỉnh tốc độ thuốc được hạn chế, hoặc là ức chế beta được ngừng hoặc tạo nhịp có thể được xem xét như là bước tiếp theo.
|
IIb
|
C
| |
Tạo nhịp chỉ để cho phép khởi đầu hoặc chỉnh liều điều trị ức chế beta khi không có chỉ định tạo nhịp thông thường không được khuyến cáo.
|
III
|
C
| |
Ở bệnh nhân có HFrEF đòi hỏi tạo nhịp và có blốc AV cao độ, CRT ưa thích hơn tạo nhịp RV được khuyến cáo.
|
I
|
A
|
274, 294, 295
|
Ở các bệnh nhân HFrEF người đòi hỏi tạo nhịp không có blốc AV cao độ, mode tạo nhịp tránh tạo ra hoặc làm trầm trong mất đồng bộ thất nên được xem xét
|
IIb
|
C
| |
AF: rung nhĩ; AV: thất nhĩ; bpm: nhịp trên phút; CRT: điều trị tái đồng bộ; ECG: điện tâm đồ; HFrEF: suy tim phân suất tống máu giảm; RV: thất phải.
aClass khuyến cáo b Mức độ bằng chứng. c Tài liệu ủng hộ các khuyến cáo
|
Tài liệu tham khảo
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