2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(03)13976-1.pdf

B-type natriuretic peptide in cardiovascular disease

Ventricular remodeling, first described in animal models of left ventricular (LV) stress and injury, occurs progressively in untreated patients after large myocardial infarction and in those with dilated forms of cardiomyopathy. The gross pathologic changes of increased LV volume and perturbation in the normal elliptical LV chamber configuration is driven, on a histologic level, by myocyte hypertrophy and apoptosis and by increased interstitial collagen. Each of the techniques used for tracking this process—echocardiography, radionuclide ventriculography, and cardiac magnetic resonance—carries advantages and disadvantages. Numerous investigations have demonstrated the value of LV volume measurement at a single time-point and over time in predicting clinical outcomes in patients with heart failure and in those after myocardial infarction. The structural pattern of LV remodeling and evidence of scarring on cardiac magnetic resonance have additional prognostic value. Beyond the impact of abnormal cardiac structure on cardiovascular events, the relationship between LV remodeling and clinical outcomes is likely linked through common local and systemic factors driving vascular as well as myocardial pathology. As demonstrated by a recent meta-analysis of heart failure trials, LV volume stands out among surrogate markers as strongly correlating with the impact of a particular drug or device therapy on patient survival. These findings substantiate the importance of ventricular remodeling as central in the pathophysiology of advancing heart failure and support the role of measures of LV remodeling in the clinical investigation of novel heart failure treatments.

Left ventricular remodeling in heart failure: current concepts in clinical significance and assessment.

Background— Combined inhibition of the angiotensin-converting enzyme (ACE) and neutral endopeptidase (NEP) may produce greater benefits in heart failure than ACE inhibition alone. Methods and Resul...

Comparison of Omapatrilat and Enalapril in Patients With Chronic Heart Failure The Omapatrilat Versus Enalapril Randomized Trial of Utility in Reducing Events (OVERTURE)

Volume 1 of Circulation provides an excellent snapshot of the understanding of the mechanisms and treatment of heart failure a half century ago. During that era, circulatory pathophysiology was at the center of investigative attention. For example, Tinsley Harrison and his group divided heart failure into “primary disorders of filling and primary disorders of emptying,”1 a forerunner of our current terms diastolic and systolic heart failure. The great Swedish clinical physiologist Gustav Nylin used 32P-labeled red blood cells for measuring cardiac output and cardiothoracic blood volume by the indicator-dilution method in normal subjects and in patients with heart failure.2 Andre Cournand’s group defined the pathophysiology of heart failure secondary to cor pulmonale, distinguished it from left ventricular failure, and compared the acute hemodynamic effects of digoxin in these 2 conditions.3 In a seminal paper, Raab and Lepeschkin extracted sympathin from the heart and established norepinephrine as the cardiac adrenergic neurotransmitter.4 In one of the earliest efforts to manage patients with chronic congestive heart failure on an outpatient basis, Vander Veer and colleagues demonstrated the effectiveness and tolerability of an oral form of the widely used parenteral diuretic mercuhydrin.5 

In the 1950s, the role of hypertrophy in the heart’s adaptation to hemodynamic overload was examined. After Laplace’s law was applied to the heart and permitted the calculation of wall stress in the human heart,6 it became clear that myocardial hypertrophy prevents excessive elevation of wall stress consequent to hemodynamic overload.7 8 In the 1960s, there was a lively debate about the mechanism of heart failure secondary to pressure overload. The question was framed as follows: “Does failure of the ventricle as a pump occur in the presence of (an) inadequate contractile mass while the contractile function of each unit (of myocardium) is normal …

Congestive Heart Failure: Fifty Years of Progress

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(00)02602-7.pdf

Comparison of vasopeptidase inhibitor, omapatrilat, and lisinopril on exercise tolerance and morbidity in patients with heart failure: IMPRESS randomised trial.

Guy Proulx

Papers

Comparison of vasopeptidase inhibitor, omapatrilat, and lisinopril on exercise tolerance and morbidity in patients with heart failure: IMPRESS randomised trial.

VEGF gene therapy fails to improve perfusion of ischemic myocardium in patients with advanced coronary disease: results of the NORTHERN trial.