Tóm tắt khuyến cáo điều chỉnh các bệnh nhân rối loạn nhịp thất và dự phòng đột tử của esc năm 2015 – P5

7. Các bệnh cơ tim 

Các bệnh cơ tim (Cardiomyopathies) là những rối loạn cơ tim được xác định bằng sự bất thường cấu trúc và chức năng của cơ tâm thất không giải thích chỉ do hẹp động mạch vành hạn chế dòng chảy hoặc các điều kiện tải bất thường.

TS Phạm Hữu Văn

[348] Chúng được phân nhóm theo đặc điểm hình thái và chức năng và được phân dưới nhóm vào các hình thái gia đình và không gia đình. Gần như tất cả các bệnh cơ tim có thể được liên kết với VA và tăng nguy cơ SCD và thay đổi theo các nguyên nhân và mức độ nghiêm trọng của bệnh.

7.1 Bệnh cơ tim giãn

7.1.1 Định nghĩa, dịch tễ học và tư liệu sống sót

DCM (dilated cardiomyopathy) được định nghĩa khi LV giãn và rối loạn chức năng tâm thu khi không có các điều kiện tải bất thường hoặc CAD đủ để gây ra suy tâm thu toàn bộ. [348] Một số khiếm khuyết di truyền gây DCM cũng có thể gây ra rối loạn chức năng tâm thu mà LV không giãn hoặc dẫn đến sẹo cơ tim chỉ là phát hiện trên CMR.

DCM thể hiện ở tất cả mọi lứa tuổi và chủng tộc. Ở người lớn, thường phổ biến hơn ở nam hơn ở phụ nữ, với tỉ lệ tổng thể 1/2500 cá thể và tỷ lệ hàng năm được ước tính theo cổ điển là 7/100 000. [349] Ở trẻ em, tỷ lệ hàng năm là 0,57/100 000. [350]

Các đột biến có khả năng di truyền bệnh lý được tìm thấy ở ít nhất 20% người trưởng thành bị DCM và giữa 10 và 20% của người thân đã có bằng chứng đối với bệnh trên tầm soát lâm sàng.[351] Sarcomere và đột biến gen protein desmosomal là phổ biến nhất, nhưng những đột biến trong lamin A/C (LMNA) và desmin thường xuyên ở bệnh nhân có bệnh dẫn truyền. [352.353] Một số ít bệnh nhân có một bệnh liên kết với X gây ra do đột biến ở gen dystrophin. Một phổ lớn các điều kiện mắc phải có thể gây ra DCM, gồm các bệnh viêm, nhiễm trùng và các bệnh hệ thống, cũng như các loại thuốc khác nhau và độc tố. Trong một số trường hợp, bệnh nhân được di truyền học, với sự phát triển của DCM sau khi tiếp xúc với các khởi kích ngoại sinh như nhiễm trùng, thuốc độc tế bào, rượu và thai nghén.

7.1.2 Phương pháp tiếp cận phân tầng nguy cơ và điều chỉnh

Phân tầng nguy cơ và điều chỉnh các bệnh nhân có bệnh cơ tim giãn

ACE = men chuyển angiotensine; CAD = bệnh mạch vành; DCM = bệnh cơ tim giãn; EPS = nghiên cứu điện sinh lý học tim; HF = suy tim; ICD = máy khử rung tim có thể cấy; LMNA = lamin A/C; LVEF = phân suất thất trái; MRA = kháng thụ thể corticoid chuyển hoá muối (meralocorticoid receptor antagonists); NSVT = nhịp nhanh thất tạm thời; NYHA = Hội tim New York ; PVS =  kích thích thất có chưng trình; SCD = đột tử tim; VA = loạn nhịp thất; VT = nhịp nhanh thất.

^aClass của các khuyến cáo.

^bMức độ bằng chứng.

^cTài liệu ủng hộ khuyến cáo.

Các yếu tố   nguy cơ ở các bệnh nhân có đột biến LMNA được khẳng định: NSVT trong quá trình theo dõi ECG lưu động, LVEF < 45% trong đánh giá đầu tiên, nam giới và đột biến không missense (chèn, xóa, hoặc đột biến ảnh hưởng đến sự cắt nối).

Tất cả các nguyên nhân tử vong ở bệnh nhân người lớn không được lựa chọn có  DCM đã giảm đáng kể với việc sử dụng các chất đối kháng hormone thần kinh và điều trị thiết bị.[358] Tỷ lệ tử vong ở trẻ em với DCM tương đối cao trong năm đầu tiên của đời sống nhưng sau đó nhiều trẻ phục hồi chức năng hoặc duy trì ổn định trên lâm sàng. [359] Các nguyên nhân chính gây tử vong tim mạch trong DCM là HF tiến triển và SCD thứ phát do VA hay ít gặp hơn do rối loạn nhịp chậm. Nhiều biến không xâm lấn đã được gợi ý như dự đoán đột tử, nhưng trong một phân tích gộp 45 nghiên cứu mới đây trên 6088 bệnh nhân, các biến chức năng và điện tâm đồ cung cấp phân biệt một cách khiêm tốn giữa các bệnh nhân có nguy cơ cao và thấp. OR cao nhất là OR cho QRS phân đoạn và sự thay đổi luân phiên sóng T; không chỉ số nào trong số các test tự trị là yếu tố dự báo quan trọng. [115] Vai trò của hình ảnh CMR đã được đánh giá trong một phân tích gộp của 9 nghiên cứu ở những bệnh nhân có bệnh cơ tim không do thiếu máu [360] và gợi ý gia tăng gadolinium trễ ở bệnh nhân có liên quan với tăng nguy cơ tử vong do tất cả các nguyên nhân, nhập viện do HF và SCD. Giá trị hơn của việc gia tăng gadolinium trễ so với các dấu hiệu tiên lượng khác cần phải được xác định.

EPS xâm lấn, PVS có thể đóng một vai trò ở bệnh nhân DCM. [115]

7.1.2.1 Các thử nghiệm điều trị khử rung tim có thể cấy trong bệnh cơ tim giãn

Một số thử nghiệm đã so sánh điều trị ICD đơn thuần hoặc kết hợp với CRT so với placebo hoặc amiodarone ở những bệnh nhân với DCM. [64.151] [154]. [313]. [316]. [317] .[354] Đại đa số đã được thực hiện trong kỷ nguyên này khi điều trị nội khoa tốt nhất đã phát triển gồm các thuốc ức chế ACE, beta-blockers và MRA. [358] RCT điều trị ICD đầu tiên đã đủ mạnh để phát hiện sự khác biệt có ý nghĩa về mặt lâm sàng trong sống sót và trong một số trường hợp (ví dụ như DEFINITE) tỷ lệ tử suất chung thấp hơn so với dự đoán trước khi tuyển chọn. Theo dõi tương đối ngắn trong một số nghiên cứu cũng như trong các tình huống khác, mối quan hệ của những sốc thích hợp để tiên lượng vẫn còn chưa chắc chắn. Chưa có nghiên cứu tiền cứu điều tra các lợi ích của ICD ở các phân nhóm bệnh căn cụ thể của DCM.

7.1.2.2 Dự phòng tiên phát

Bốn thử nghiệm ngẫu nhiên [CArdiomyopathy Trial (CAT), [361] AMIOdarone Versus Implantable cardioverter-defibrillator: Randomized Trial in patients with non-ischaemic dilated cardiomyopathy and asymptomatic non-sustained ventricular tachycardia (AMIOVIRT),[354] DEFINITE [316] and SCD-HeFT [64] kiểm tra ảnh hưởng điều trị ICD đơn thuần trong phòng ngừa SCD tiên phát. Nghiên cứu tiếp theo, COMPANION, [313] so sánh CRT-D, CRT-P và điều trị amiodarone ở bệnh nhân suy tim tiến triển (NYHA class III hoặc IV) và khoảng QRS 120 ms. Các nghiên cứu khác nhau về thiết kế: CAT, AMIOVIRT và DEFINITE chỉ đăng ký những bệnh nhân DCM không do thiếu máu cục bộ, trong khi SCD-HeFT và COMPANION bao gồm những bệnh nhân có rối loạn chức năng LV do thiếu máu cục bộ và không thiếu máu cục bộ. Chỉ COMPANION thấy giảm một cách có ý nghĩa thống kê trong đột tử với ICD so với điều trị nội khoa tối ưu. Tất cả các nguyên nhân tử vong ở nhóm CRT-D thấp hơn so với nhóm điều trị bằng thuốc [HR 0.50 (95% CI 0.29, 0.88), P = 0,015], nhưng đã được liên kết với nguy cơ cao hơn đáng kể các biến cố có hại trung bình hoặc nặng một cách có ý nghĩa từ bất ký nguyên nhân (69% so với 61% ở nhóm điều trị nội khoa, P = 0,03). Phân tích gộp 5 thử nghiệm phòng ngừa tiên phát (1854 bệnh nhân có DCM không thiếu máu cục bộ) cho thấy giảm một cách có ý nghĩa thống kê 31% trong tử suất do tất cả các nguyên nhân cho ICD so với điều trị nội khoa [RR 0.69 (95% CI 0.55, 0.87), P = 0,002 ] [317]. Hiệu quả nảy duy trì khi COMPANION được loại trừ [RR 0.74 (95% CI 0,58, 0,96), P = 0.02] [317]. Các khuyến cáo cho điều trị ICD trong hướng dẫn này được dựa trên những phân tích này.

7.1.2.3 Dự phòng thứ phát

Ba thử nghiệm (AVID,[153] CASH [152] và CIDS  [151]  (xem ở Bảng 5) kiểm tra điều trị ICD cho phòng ngừa thứ phát ở bệnh nhân có bệnh sử ngưng tim được thoát hoặc VT có triệu chứng. Trong nghiên cứu CASH, bệnh nhân được ngẫu nhiên ngay khởi đầu để nhận ICD hoặc một trong 3 thuốc: amiodarone, metoprolol hoặc propafenone, nhưng về phía propafenone đã phải chấm dứt sớm do tử vong tăng lên. Các phân tích cuối cùng gộp dữ liệu từ phía amiodarone và metoprolol. Ba thử nghiệm đăng ký tổng cộng 1.963 bệnh nhân, trong đó chỉ có 292 (14,8%) có bệnh cơ tim không thiếu máu cục bộ. Cả AVID và CIDS đều không thông báo giảm có ý nghĩa trong tử suất do tất cả các nguyên nhân với điều trị ICD trong phân nhóm các bệnh nhân bệnh cơ tim không do thiếu máu cục bộ; kết quả cho phân nhóm này đã không được báo cáo trong nghiên cứu CASH. Nghiên cứu CASH cũng khác biệt với AVID và CIDS trong đó LVEF trung bình cao hơn và 50% số bệnh nhân đã nhận được hệ thống ICD thượng tâm mạc. Trong một phân tích tiếp theo, trong đó tư liệu từ AVID và CIDS được gộp chung, có 31% giảm không có ý nghĩa trong tử suất do tất cả các nguyên nhân liên quan đến điều trị nội khoa. [154]

7.1.2.4 Tử suất nguyên nhân cụ thể

Một vài nghiên cứu đã kiểm tra chẩn đoán hoặc điều trị trong các phân nhóm DCM cụ thể. Các đặc trưng nhất khoảng 5-10% bệnh nhân có các bệnh gây ra do đột biến ở gen LMNA. [71. 352] Bệnh tim liên quan đến LMNA cho thấy penetrance (Mức độ mà một gen đặc biệt hoặc thiết lập các gen được thể hiện trong các kiểu hình của cá nhân mang theo nó, được đo bằng tỷ lệ của các biểu hiện kiểu hình đặc trưng. Vì giảm penetrance, cá nhân của các kiểu gen khác nhau có thể có kiểu hình giống nhau. Người dịch) liên quan với tuổi với rối loạn nhịp nhĩ khởi đầu sớm tiếp theo bằng sự phát triển bệnh dẫn truyền và nguy cơ đột tử cao, thường chỉ với giãn LV và suy chức năng taam thu nhẹ. Trong đăng ký đa trung tâm 269 người mang đột biến LMNA, phân tích đa biến chứng minh NSVT trong theo dõi điện tâm đồ lưu động, LVEF < 45% trong đánh giá đầu tiên, nam giới và các đột biến không missense (chèn-xóa / cắt hoặc đột biến ảnh hưởng đến  chỗ nối) là các yếu tố nguy cơ độc lập cho VA ác tính. [71] VA ác tính chỉ xảy ra ở những người có ít nhất hai trong số các yếu tố nguy cơ và có nguy cơ cộng dồn cho mỗi yếu tố nguy cơ bổ sung.

7.1.2.5 Điều chỉnh các rối loạn nhịp thất trong bệnh cơ tim giãn

Bệnh nhân DCM và VA tái phát cần được điều trị nội khoa tối ưu bằng các thuốc ức chế men chuyển, thuốc chẹn bêta và MRA phù hợp với các nguyên tắc của ESC cho HF mãn tính. [8] Các yếu tố thúc đẩy VA một cách rõ ràng cho (thuốc thúc đẩy loạn nhịp, hạ kali máu) hoặc các bệnh đi kèm (ví dụ như bệnh tuyến giáp) thúc đẩy VA nên tầm soát và điều trị khi có thể. Ở những bệnh nhân trước đây ổn định với khởi phát VA mới, chụp động mạch vành nên được xem xét ở những bệnh nhân với nguy cơ cao trung gian cho CAD. Amiodarone cần được xem xét ở những bệnh nhân có ICD có các sốc phù hợp tái phát mặc dù đã lập trình thiết bị tối ưu, [229] nhưng không nên được sử dụng để điều trị các cơn NSVT không triệu chứng. Việc sử dụng các thuốc chẹn kênh natri và dronedaron không được khuyến cáo ở những bệnh nhân có suy chức năng LV vì những tác dụng thúc đẩy loạn nhịp tiềm tàng của thuốc. [129.152.357.362.363]

7.1.2.6 Triệt phá nhịp nhanh thất

Các nền cho VT trong DCM rất phức tạp, phản ánh nhiều nguyên nhân của bệnh. Nghiên cứu đánh giá các chiến lược triệt phá khác nhau trong báo cáo DCM, khi tốt nhất, thành công khiêm tốn, không cải thiện khi lập bản đồ thượng tâm mạc và nội tâm mạc được thực hiện. Trong một nghiên cứu đăng ký gần đây so sánh 63 bệnh nhân bệnh cơ tim không thiếu máu cục bộ và 164 bệnh nhân có rối loạn chức năng LV do thiếu máu cục bộ,  [208] triệt phá VT lâm sàng chỉ đạt được ở 18,3% bệnh cơ tim không do thiếu máu cục bộ. Như vậy  triệt phá qua catheter VT ở bệnh nhân DCM nên dành cho những bệnh nhân có một cơ chế VT rõ ràng (ví dụ như vào lại nhánh bó) và thực hiện tại các trung tâm có kinh nghiệm.

7.2 Bệnh cơ tim phì đại

7.2.1 Định nghĩa, dịch tễ học và tư liệu sống sót

HCM (Hypertrophic cardiomyopathy) được đặc trưng bằng sự gia tăng độ dày thành LV nhưng không chỉ giải thích do điều kiện tải LV bất thường. [116] Định nghĩa này áp dụng đối với trẻ em và người lớn và không đưa ra được các giả định về bệnh căn, nhưng đối với các mục đích của hướng dẫn này, các khuyến cáo về việc dự phòng SCD áp dụng cho bệnh nhân không có bệnh về chuyển hóa, thâm nhiễm hoặc các bệnh khác có bệnh sử tự nhiên và điều trị rất khác biệt.

Các nghiên cứu ở bắc Mỹ, châu Âu, châu Á và châu Phi báo cáo một tỷ lệ không giải thích được phì đai LV ở khoảng 0,02-0,23% ở người lớn, với tần số thấp hơn nhiều  ở bệnh nhân < 25 tuổi. [116] Trong khi HCM được di truyền phổ biến nhất như một đặc điểm di truyền mang tính trạng trội, hầu hết các nghiên cứu báo cáo sự vượt trội nhỏ ở nam giới và tần số HCM như nhau trong các nhóm chủng tộc khác nhau.[116] Nhìn chung tỷ lệ tử vong tim mạch hàng năm và tỷ lệ tử vong hoặc phóng điện ICD phù hợp cho VT/VF ở người lớn HCM không được lựa chọn là 1-2 và 0,81%, tương ứng. [364.365] Các nguyên nhân tử vong tim mạch lớn khác gồm HF, thuyên tắc huyết khôi và blốc AV.

(Còn nữa)

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