CHF results when heart is not able to meet the demands of circulation causing insufficient blood flow. These patients are at higher risk of arterial and venous thrombosis.
Throughout history many renowned researchers and health care professionals have contributed to the understanding, definition, and recognition of thrombosis in Heart Failure patients.[1][2][3]
Prognosis appeared better in Anticoagulated patient.
1960s - 1970s
Retrospective analysis and Autopsy findings showed thromboembolism as an etiology.
1980s - 1990s
Better understanding of hypercoaugubilty in Heart failure patients. In 1987, the landmark CONSENSUS-I study showed the unequivocal survival benefits of enalapril in patients with severe heart failure.
2000-
Role of Aspirin in heart failure patients is studied.
Stagnation of blood flow, disorder in vascular wall, and blood coagulation system are known factors that participate in the thrombosis formation, and its evident that Heart failure is often accompanied by hypercoaguble state[4][5][6].
Heart failure is the most frequent cause of hospitalization in patient aged 65 and above.[10]Heart failure is one of the most important public health problems, affecting an approximate half million patients in United States, with more than 550,000 new cases each year, and many more worldwide[11][4].
The incidence is expected to increase further in the next two decade as more number of people are surviving after myocardial infarction[12].
Death is the ultimate complication that can happen in heart failure patients having thrombosis. In the ATLAS (Assessment of Treatment with Lisinopril and Survival) trial[13], there were many Heart failure patients who underwent autopsy, providing an unique opportunity and answering many questions about the cause of death.
Various trials have been conducted to suggest surrogate markers of heart failure.
Cause of death in autopsied Heart failure patients: ATLAS Trial[edit | edit source]
The following Table shows the comparative data from various studies, each showing the probability of a thromboembolic events in Heart Failure patients.
Figures mentioned under CVA, MI, PE, TTE represents per 100 patient-years. Abbreviations Used: TTE, Total Thromboembolic event rate; NR, not reported; V-HeFT I and II Vasodilator-Heart Failure Trials; SAVE, Survival and Ventricular Enlargement; SOLVD, Studies of Left Ventricular Dysfunction; WASH, Warfarin/Aspirin Study of Heart Failure;HELAS,Heart Failure Long-Term Antithrombotic Study;IHD, Ischemic Heart Disease;DCM, Dilated CardiomyopathySCD-HeFT, Sudden Cardiac Death in Heart Failure Study.
The Warfarin and Antiplatelet Therapy in Chronic Heart Failure (WATCH[22]) trial was the first modern RCT to study warfarin in patients with heart failure. The trial showed a reduction of nonfatal stroke events with warfarin over aspirin or clopidogrel.
In the ARixtra for ThromboEMbolISm prevention in a medical indications study (ARTEMIS[23]) trial in acutely ill medical patients, fondaparinux significantly reduced the risk of total venous thromboembolism, without increasing bleeding risk compared with placebo.
In the Survival and Ventricular Enlargement (SAVE[24]) Trial,which enrolled patients with left ventricular dysfunction after MI, the VTE annual rate (fatal and nofatal stroke) was 1.5%.
↑HARVEY WP, FINCH CA (1950). "Dicumarol prophylaxis of thromboembolic disease in congestive heart failure". N Engl J Med. 242 (6): 208–11. doi:10.1056/NEJM195002092420603. PMID15403339.
↑GRIFFITH GC, STRAGNELL R, LEVINSON DC, MOORE FJ, WARE AG (1952). "A study of the beneficial effects of anticoagulant therapy in congestive heart failure". Ann Intern Med. 37 (5): 867–87. PMID12986600.CS1 maint: Multiple names: authors list (link)
↑ 6.06.1Sbarouni E, Bradshaw A, Andreotti F, Tuddenham E, Oakley CM, Cleland JG (1994). "Relationship between hemostatic abnormalities and neuroendocrine activity in heart failure". Am Heart J. 127 (3): 607–12. PMID8122609.CS1 maint: Multiple names: authors list (link)
↑ 13.013.1Uretsky BF, Thygesen K, Armstrong PW, Cleland JG, Horowitz JD, Massie BM; et al. (2000). "Acute coronary findings at autopsy in heart failure patients with sudden death: results from the assessment of treatment with lisinopril and survival (ATLAS) trial". Circulation. 102 (6): 611–6. PMID10931799.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑Kannel WB, Wolf PA, Verter J (1983). "Manifestations of coronary disease predisposing to stroke. The Framingham study". JAMA. 250 (21): 2942–6. PMID6227757.CS1 maint: Multiple names: authors list (link)
↑Dunkman WB, Johnson GR, Carson PE, Bhat G, Farrell L, Cohn JN (1993). "Incidence of thromboembolic events in congestive heart failure. The V-HeFT VA Cooperative Studies Group". Circulation. 87 (6 Suppl): VI94–101. PMID8500246.CS1 maint: Multiple names: authors list (link)
↑Loh E, Sutton MS, Wun CC, Rouleau JL, Flaker GC, Gottlieb SS; et al. (1997). "Ventricular dysfunction and the risk of stroke after myocardial infarction". N Engl J Med. 336 (4): 251–7. doi:10.1056/NEJM199701233360403. PMID8995087.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑St John Sutton M, Pfeffer MA, Moye L, Plappert T, Rouleau JL, Lamas G; et al. (1997). "Cardiovascular death and left ventricular remodeling two years after myocardial infarction: baseline predictors and impact of long-term use of captopril: information from the Survival and Ventricular Enlargement (SAVE) trial". Circulation. 96 (10): 3294–9. PMID9396419.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)