Heart failure etiology

Differentiate between the common underlying etiologies of heart failure, including ischemic, non-ischemic, and idiopathic causes. 

Heart failure patients exist in one of two clinical states. When a patient s volume status and symptoms are stable, their HF condition is said to be compensated. In situations of volume overload or other worsening symptoms, the patient is considered decompensated. Acute decompensation can be precipitated by numerous etiologies that can be grouped into cardiac, metabolic, or patient-related causes (Table 3-3).5... 

High-risk patients Hypertensive patients at risk of excessive hypotension include those with the following concurrent conditions or characteristics Heart failure, hyponatremia, high-dose diuretic therapy, recent intensive diureses or increase in diuretic dose, renal dialysis, or severe volume or salt depletion of any etiology. Single doses of enalaprilat as low as 0.2 mg have produced excessive hypotension in normotensive patients with these diagnoses. Because of the potential for an extreme hypotensive response in these patients, initiate therapy under very close medical supervision. The... 

The results of MADIT II were met with some skepticism, but later confirmed by the recent Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) [24]. This study evaluated the benefit of ICD therapy versus amiodarone or placebo as primary prevention in over 2,500 patients with stable NYHA class II or III heart failure and EF < 35%, without the requirement for NSVT or EPS. Patients with both ischemic and nonischemic etiologies for cardiomyopathy were included. Over a follow-up of 4 years, there was no benefit of amiodarone over placebo for overall mortality, but ICD therapy resulted in a significant 23% reduction in overall mortality [p = 0.007] (Fig. 3.5). The benefit of ICD therapy was comparable for ischemic and nonischemic cardiomyopathy. 

Heart failure is a progressive syndrome, and optimal pharmacologic management is based on a detailed diagnosis, determination of the etiology, characterization of the clinical syndrome (systolic vs. diastolic) and careful monitoring of the response to pharmacologic therapy. There is a need to modify treatment in accordance with the patient s response to therapy. 

Fig. 2.1 Schematic representation of the mechanisms involved in the development of heart failure due to different etiologies.

To date, proteomic investigations into human heart disease have centered on dilated cardiomyopathy (DCM). DCM is a disease of unknown etiology, characterized by impaired systolic function resulting in heart failure. Known contributory factors of DCM are viral infections, cardiac-specific autoantibodies, toxic agents, genetic factors, and sustained alcohol abuse. As many as 100 cardiac proteins... 

Thiamin that is not bound to plasma proteins is rapidly filtered at the glomerulus. Diuresis increases the excretion of the vitamin, and patients who are treated with diuretics are potentially at risk of thiamin deficiency. Some of the diuretics used in the treatment of hypertension may also inhibit cardiac (and other tissue) uptake of thiamin, thus further impairing thiamin status, which may be a factor in the etiology of heart failure (Suter and Vetter, 2000). 

The clinical manifestations of heart failure vary considerably and depend on many factors, including the (1) clinical characteristics of the patient, (2) extent and rate at which the heart s performance becomes abnormal, (3) etiology of the heart disease, (4) concomitant co-morbidities, and (5) distribution of the abnormal cardiac function. The severity of impairment can range from mild-— manifested clinically only during stress—to advanced, in which cardiac pump function is unable to sustain life without external support. 

The first step in the management of chronic heart failure is to determine the etiology (see Table 14—1) and/or any precipitating factors. Treatment of underlying disorders such as anemia or hyperthyroidism may obviate the need for treatment of heart failure. Patients with valvular diseases may derive significant benefit from valve replacement or repair. Revascularization or anti-ischemic therapy in patients with coronary disease may reduce heart failure symptoms. Drugs that aggravate heart failure (see Table 14—3) should be discontinued, if possible. 

The beneficial effect of ACE inhibitors on mortality has been documented conclusively, with numerous trials showing a 20% to 30% relative reduction in mortality with ACE inhibitor therapy compared with placebo. A long-term (12-year) follow-up of the Studies of Left Ventricular Dysfunction (SOLVD) prevention and treatment trials demonstrated sustained survival benefits in patients treated with enalapril. In addition to improving survival, ACE inhibitors also reduce the combined risk of death or hospitalization, slow the progression of heart failure, and reduce the rates of reinfarction.The benefits of ACE inhibitor therapy are independent of the etiology of heart failure (ischemic versus nonischemic) and are observed in patients with mild, moderate, or severe symptoms. ACE inhibitors clearly are superior to vasodilator therapy with hydralazine-isosorbide dinitrate. ... 

A careful history and physical examination are key components in the diagnosis of decompensated heart failure. The history should focus on the potential etiologies of heart failure the presence of any precipitating factors onset, duration, and severity of symptoms and a careful medication history. Important elements of the physical examination include vital signs, cardiac auscultation for heart sounds and murmurs, pulmonary examination for the presence of rales, the presence of peripheral edema, and weight. The JVP is a reliable indicator of the patient s volume status and should be evaluated carefully on admission and followed closely as an indicator of the efficacy of diuretic therapy. 

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