History and exam

Key diagnostic factors

The most common symptom of left-sided heart failure. May occur with exertion (New York Heart Association [NYHA] II-III) or, in more severe cases, at rest (NYHA IV). This is considered a minor criterion for the diagnosis of heart failure (Framingham criteria).

A major Framingham criterion for the diagnosis of heart failure.

A major Framingham criterion for the diagnosis of heart failure.

Cardiomegaly is a major Framingham criterion for the diagnosis of heart failure. Left ventricular dilation or hypertrophy are common findings.

A major Framingham criterion for the diagnosis of heart failure.

A major Framingham criterion for the diagnosis of heart failure.

Orthopnea worsens immediately after lying down, because of a sudden increase in venous return; that is, preload. Paroxysmal nocturnal dyspnea occurs several hours after the patient lies down to sleep; it results from the central redistribution of extravascular fluid that progressively increases the venous return.

Increased frequency of uresis occurs several hours after the patient lies down to sleep; it also results from the central redistribution of extravascular fluid that augments the amount of circulating blood cleared from the kidneys.

Other diagnostic factors

A minor Framingham criterion for the diagnosis of heart failure.

A symptom of poor coronary perfusion.

A minor Framingham criterion for the diagnosis of heart failure; may cause abdominal discomfort/distention and nausea.

A minor Framingham criterion for the diagnosis of heart failure.

A minor Framingham criterion for the diagnosis of heart failure.

A minor Framingham criterion for the diagnosis of heart failure.

Symptom of poor tissue (muscle) perfusion.

This may be the result of frequent ectopic supraventricular or ventricular beats or may reflect paroxysms of atrial flutter/fibrillation; permanent atrial fibrillation may or may not cause palpitations.

Symptom of poor tissue (brain) perfusion.

Risk factors

The link between MI and risk of heart failure development is strongly and consistently supported by the literature. MI, which confers at least a 15-fold increased risk, is the single most potent risk factor for developing heart failure.[9][10][11][12][13][14]

Diabetes mellitus has been associated with a 3- to 5-fold increase in the risk of developing heart failure,[10][11][12][14][15][16] with the highest increase in relative risk found among women[10][14] and people with asymptomatic left ventricular dysfunction.[15] Even a slight increase of 1% in hemoglobin A1C has been linked to a greater than 10% risk of hospitalization for heart failure or death.[17]

Lipid abnormalities have been linked to increased risk for heart failure.[18][19][20] Compared with men with ratios of total cholesterol:HDL cholesterol of less than 5, in one study men with ratios of 5 to 9.9 had a 1.5-times greater incidence of heart failure, and men with ratios of greater than 10 had a nearly 5-times greater incidence of heart failure.[18] In the same study, women with ratios greater than 10 had more than 6-times greater incidence of heart failure than women with ratios less than 5.[18] In one clinical trial of patients with coronary artery disease, lipid lowering was associated with a 21% reduction in the risk of developing heart failure.[21]

Increasing age has been consistently linked to a higher risk of developing heart failure.[3][9][10][11][12][13][22] In the Framingham cohort, the incidence of heart failure increased steadily with increasing age.[10] In a cohort of people over age 65 years, every 5-year incremental increase in age was associated with a hazard ratio of 1.37.[12] In another study, the incidence rate of heart failure among the oldest people (age >80 years) was double that of the youngest people (age 65 to 69 years).[22]

Male sex has been consistently linked to a higher risk of developing heart failure.[3][9][10][11][12][13][14][22] In the Framingham cohort, women had a one third lower incidence of heart failure than men and male sex was associated with a hazard ratio of 1.34.[10][12][14] In other studies the incidence among males is 2 to 4 times that of females.[9][22] In the National Health and Nutrition Examination Survey (NHANES I) study, which followed a cohort of 13,643 people for an average of 19 years, being male was associated with a relative risk of heart failure of 1.24.[23]

Hypertension has consistently been linked to an increased risk of heart failure in the literature and confers a 2- to 3-fold increase in risk of developing heart failure.[9][10][11][12][13][14][24] Elevated systolic blood pressure, elevated diastolic blood pressure, and elevated pulse pressure have all been associated with increased risk for heart failure.[25][26] Among the Framingham cohort, a one standard deviation (20 mmHg) increase in systolic blood pressure was associated with a 56% increased risk for heart failure, a one standard deviation (10 mmHg) increase in diastolic blood pressure was associated with 24% increased risk, and a one standard deviation (16 mmHg) increase in pulse pressure was associated with a 55% increase in risk.[25]

Moderate-to-severe asymptomatic left ventricular dysfunction (ejection fraction [EF] <40%) has been associated with a hazard ratio of heart failure of 7.8, while mild asymptomatic left ventricular dysfunction (EF 40% to 50%) has been associated with a hazard ratio of 3.3.[27]

Cocaine abuse has been strongly associated with the development of heart failure in a variety of care settings.[28][29][30]

Doxorubicin and cyclophosphamide can cause myocardial damage leading to left ventricular dysfunction and heart failure.[38][39] These chemotherapeutic agents increase risk for heart failure both during acute treatment and for several months after treatment has ended, with increasing risk with increasing cumulative dose.[40][41] In addition, trastuzumab, a recombinant DNA-derived humanized monoclonal antibody used widely in the treatment of breast cancer, is also associated with the development of cardiomyopathy. The antihypertensive medication doxazosin has been linked to an increased risk of heart failure. Thiazolidinediones (a class of drug used for the treatment of diabetes) have been associated with an increased risk of heart failure.

Mediastinal irradiation can cause direct myocardial damage leading to left ventricular dysfunction and heart failure both during acute treatment and for several years after treatment has ended.

Left ventricular hypertrophy on electrocardiogram has been associated with a higher risk of heart failure, with highest relative risk among younger people.[42]

Renal insufficiency, defined by elevated serum creatinine (over 1.5 mg/dL in men and 1.3 mg/dL in women) or reduced creatinine clearance (less than 60 mL/minute), has been linked to increased risk for development of heart failure. Compared with subjects with creatine of less than 1.1 mg/dL, subjects with creatinine of 1.3 to 1.49 mg/dL had almost double the risk of developing CHF, subjects with creatine of 1.5 to 1.69 mg/dL had almost triple the risk, and those with creatine greater than 1.7 mg/dL had almost quadruple the risk.[44][45]

Cardiac valvular abnormality was associated with an odds ratio of heart disease of 2.43 among men and 3.47 among women in a multivariate profile based on the Framingham cohort.[46] Valvular abnormalities create pressure overload (e.g., aortic stenosis, mitral stenosis) or volume overload (e.g., mitral regurgitation), which are initially compensated for by mechanisms such as ventricular hypertrophy or ventricular dilation.[47] Ventricular remodeling alters cardiac contractility and increases the risk of heart failure.

Sleep-disordered breathing has been linked with increased risk of heart failure in multiple studies.[48][49][50]

In the Framingham cohort, elevated plasma homocysteine levels were linked with a roughly three quarter increased risk for developing heart failure.[54]

TNF-alfa is a pro-inflammatory cytokine associated with myocyte death and cardiac dysfunction.[55] IL-6 is a similar pro-inflammatory cytokine.[56]

Among the Framingham cohort, an increase of 5 mg/dL in CRP level was associated with over a 2-fold increase in risk of heart failure.[56] People who also had elevated serum IL-6 and TNF-alfa values had a 4-fold increase in risk of heart failure.[56]

IGF-1 has been shown to have positive inotropic effects and to decrease the rate of cellular apoptosis.[57][58] IGF-1 has also been tentatively linked to vasodilation, which may improve cardiac emptying.[59] Among the Framingham cohort, patients with a serum IGF-1 level below 140 mg/L had double the risk of developing heart failure.[60]

In the Framingham cohort, increased levels of plasma B-type natriuretic peptide (BNP) and N-terminus of the atrial natriuretic peptide prohormone (N-ANP) were associated with an increased risk of heart failure. BNP levels above the 80th percentile (20 picograms/mL for men and 23.3 picograms/mL for women) were associated with a 3-fold increase in heart failure risk.[61]

The risk-factor-adjusted hazard ratio for heart failure in an asymptomatic population was 1.47 per 1 standard deviation increase in left ventricular end-diastolic diameter and 1.43 per 1 standard deviation increase in left ventricular end-systolic dimension.[27]

In one cohort, those who developed heart failure had an initial average left ventricular mass/height of 106 g/m, versus 88 g/m among those who did not develop heart failure.[27][62][63]

Alternations in the E to A wave ratio, both low and high, have been associated with heart failure risk, with those with the lowest E to A wave ratio (<0.7) having a relative risk of 1.88 and those with the highest E to A wave ratio (>1.5) having a relative risk of 3.50.[27][63]

Several polymorphisms have been linked with an increased risk of developing heart failure: for example, a deletion of 4 amino acids in position 322 to 325 of the gene coding for a2C-adrenergic receptors (a2C Del322-325) in sympathetic nerve endings in the heart has been studied as a possible link to the development of heart failure. A second polymorphism that was evaluated as a candidate for developing heart failure is a change in position 389 of the gene for beta1-adrenergic receptors (b1Arg389) on myocytes. In the same study, patients who were homozygous for this deletion had a 10-fold increase in risk of developing heart failure.[64]

Atrial fibrillation increases the risk of thrombo-embolic events (e.g., stroke) and may lead to a worsening of symptoms. Atrial fibrillation may also serve as a predictor of mortality, or lead to tachycardiomyopathy, though evidence is less clear.[1]

For example, thyrotoxicosis and hypothyroidism. Thyroid disorders are treatable, but are linked to sinus tachycardia, bradycardia, and atrial tachycardia/flutter/fibrillation.[1]

Anemia is a strong risk factor and prognostic marker of poor survival. A high prevalence of iron deficiency has been reported in heart failure.[65] Iron deficiency in heart failure is due to gastrointestinal or genitourinary blood loss related to the use of antiplatelet drugs and/or oral anticoagulation, impaired nutrition, malabsorption, and reduced intracellular uptake of iron.[66][67]

The National Health and Nutrition Examination Survey (NHANES I) study found that low socioeconomic status (as indicated by less than high school education) was associated with a relative risk of heart failure of 1.22 (population attributable risk 8.9%).[23]

In contrast to the strong influence of cocaine abuse on the development of heart failure, the literature on the importance of smoking independent of other factors is conflicting.[10][23][31][32] In the Framingham cohort, cigarette smoking was not linked with increased incidence of heart failure except among men over age 64 years.[10] In other studies, tobacco use has been associated with a relative risk of heart failure of 1.59 and of 1.51 (smoking <15 cigarettes a day) to 2.31 (smoking 15 or more cigarettes a day).[23][31]

Current data strongly support a relationship between excess alcohol consumption and the development of heart failure.[33][34][35] This may be related to both direct myocardial toxicity of alcohol and the higher risk of hypertension development. However, the data also suggest a possible weakly protective effect of moderate alcohol consumption.[36] This may be related to lower risk of diabetes and myocardial infarction, and favorable changes in the lipid profile, platelet function, and blood clotting associated with moderate alcohol intake.

The National Health and Nutrition Examination Survey (NHANES) found the relative risk for a 100-mmols/day increase in sodium intake was 1.26.[37]

Consumption of five or more cups of coffee a day has been associated with a relative risk of heart failure of 1.11.[31]

Excess body weight is now an established risk factor for the development of heart failure. Among a subset of the Framingham cohort, the risk of heart failure increased by 5% for men and 7% for women with each increase of 1 in body mass index; obese subjects (body mass index 30 or above) had a risk of heart failure double that of nonobese subjects.[43]

Tachycardia-induced cardiomyopathy has been well described in the literature. Among the Framingham cohort, an increase in heart rate of 10 beats per minute was linked with a greater than 10% increased risk of developing heart failure.[46]

Risk is double among depressed compared with nondepressed older people.[51][52]

Although no link between microalbuminuria and the development of heart failure has been established, microalbuminuria was linked with a 3-fold increased risk of heart failure hospitalization in the Heart Outcomes Prevention Evaluation study.[53]

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