Heart failure affects about 5 million Canadians and Americans and the incidence is expected to increase in the next few years as an aging population increases in size and morbidity. One kind of heart failure is caused by weak ventricular pumping. A second kind in patients with a normal left ventricular ejection fraction is due to poor ventricular relaxation and passive stiffness that limits filling. A third kind of heart failure is caused by defective valves that limit outflow and/or allow flowback. When the mitral valve leaks, for example, the left ventricle has to work harder to maintain cardiac output. The ventricle enlarges and if the heart circulation is adequate, pumping action is strong, but some of the blood flows back through the left atrium into the pulmonary venous system.
When I was a medical student heart failure was a common problem in the medical wards, and we became expert at recognizing and treating this condition. The majority of heart failure patients had heart valve disease from rheumatic fever. These patients have almost disappeared from medical wards. They have been replaced by patients whose heart failure is caused by damage to heart muscle, usually by coronary artery disease or small vessel disease caused by smoking and diabetes. The signs of advanced heart failure are obvious when you do a careful physical examination. A plain chest X-Ray will show heart enlargement and fluid in the lungs when heart failure is advanced
Smith described heart failure (HF) due to pump failure: ”The HF syndrome consists of symptoms of fatigue, shortness of breath, and development of pulmonary congestion and peripheral edema. The syndrome is also associated with cardiac rhythm disorders and premature mortality related to myocardial failure or to sudden cardiac rhythm disturbances. In addition to these symptoms, patients with HF due to prior myocardial damage are at risk for progressive ventricular dilation and a decrease in systolic function, a process known as ventricular remodeling…Hemodynamic abnormalities, including elevation of the pressures within the heart, increases in systemic vascular resistance, and diminution in cardiac output (CO)...a number of neuroendocrine abnormalities were identified, including activation of the sympathetic nervous system and increases in hormones, including norepinephrine, angiotensin II, renin, aldosterone, vasopressin, and, most recently, B-type natriuretic peptide (BNP). In the past several years, there has been an increasing awareness of the effects of conduction abnormalities associated with abnormal myocardial function and the unfavorable prognostic significance of these findings.”
Redfield described diastolic heart failure: “Studies have established that 40 percent to 50 percent of patients with heart failure have a normal ejection fraction ( 50 percent) without primary valve disease, a clinical syndrome that is commonly referred to as "diastolic" heart failure.”
Heart failure usually is a slow and progressive process.The heart muscle weakens or stiffens over many years and leaves patients exhausted and disabled. Often, failure is precipitated by a heart attack that leaves the heart muscle damaged and less effective as a pump. Active heart muscle is replaced by inactive scar tissue that may limit the elasticity of a damaged ventricular and limit that amount of blood that can enter during diastole. Reducing filling capacity and weak pumping combine to reduce cardiac output. Coronary angioplasty and bypass surgery relieve heart attack symptoms, but do not repair the heart damage or stop heart failure. Surgical interventions may save lives of patients who have heart attacks, but many survivors have damaged hearts that will eventually fail. Heart failure can be treated with ACE inhibitors and beta-blockers; improvement may take several months to develop.
In his review of the history of managing heart failure, Yancy stated: ”The prevailing hypothesis until the early 1990s was based in large measure on a hemodynamic understanding of heart failure, with an emphasis on abnormally increased loading conditions. Modest benefit in the natural history of heart failure was established with the use of vasodilator therapy, specifically, isosorbide dinitrate and hydralazine. Beginning in the early 1990s, however, the introduction of angiotensin-converting enzyme (ACE) inhibitors led to the first major reductions in morbidity and mortality due to heart failure. Targeting the renin-angiotensin-aldosterone system with ACE inhibitors resulted in a significant reduction in the risk of death due to heart failure. Approximately a 20% survival advantage was documented in well-designed placebo-controlled, randomized clinical trials. Additional studies, initiated in Northern Europe in the 1970s, ultimately demonstrated that targeting the sympathetic nervous system with beta-adrenergic receptor blockers was beneficial. This realization that a perturbed neurohormonal environment is central to the progression of left ventricular dysfunction - this "neurohormonal hypothesis" has since been proven and is now the premise for pharmacologic interventions in heart failure. Beta-adrenergic blockade in heart failure is an effective treatment strategy when correctly applied in the appropriate patient.
The initiation of low-dose therapy with beta-adrenergic receptor blockers, with careful and gradual titration in a euvolemic patient with heart failure, has proven to be well tolerated across all classes of disease severity and has led to substantial reductions in morbidity and mortality due to heart failure. The consequence of comprehensive neurohormonal blockade has resulted in a near 50% reduction in the risk of death due to heart failure. The public health implications are staggering, and efforts are under way to maximize the use of these agents. The validity of the neurohormonal hypothesis was further supported by the striking benefit of low-dose aldosterone blockade observed in the Randomized Aldactone Evaluation Study (RALES) trial, which reported a nearly 35% improvement in the risk of death in advanced heart failure in patients already treated with ACE inhibitor therapy.”
Heart muscle increases in bulk in response to increased cardiac load. For many years this heart enlargement was thought to be a result of demand for increased blood flow and increased blood pressure but more recently the effect of chemical mediators is appreciated: vasoactive peptides, catecholamines, cytokines and growth factors all contribute to cardiac hypertrophy. Inhibition of the angiotension II receptors reduces cardiac hypertrophy and progression towards heart failure. AT receptors act as heart muscle work-sensors, converting mechanical stress into chemical signals.
Jeejeebhoy suggested some potential nutritional strategies in heart failure: Protein-energy malnutrition is present in 50% of people with CHF. Thiamine is supplemented because diabetics and patients on diuretics may become thiamine deficient. Diabetic patients lose thiamine in their urine and must take high dose supplements. Thiamine deficiency results in reduced glucose oxidation. Carnitine also aids glucose oxidation. Carnitine makes free CoA available in the cell which in turn promotes the oxidation of pyruvate derived from glycolysis by activating the enzyme pyruvate dehydrogenase. Feeding L-Carnitine 2 gm/day improved outcome in patients with cardiac failure.
CoQ10, or ubiquinone, 2 mg/kg/d for 52 weeks reduced hospital stays and episodes of pulmonary edema in patients with heart failure. Mitochondrial function is reduced in the failing heart and calcium accumulates because heart cells lack energy to pump it out efficiently. Taurine with antioxidants protects mitochondria and myocytes from injury. In cardiomyopathic hamsters, taurine reduced muscle calcium and cardiac damage.
Cardiac assist devices are considered when HF persists after an adequate trial of drug therapy. Implantable cardioverter defibrillators (ICDs) are used to prevent sudden cardiac death from ventricular arrhythmias.
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