History and exam
Key diagnostic factors
common
dyspnea
The most common symptom of left-sided HF. 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 HF (Framingham criteria).
neck vein distension
A major Framingham criterion for the diagnosis of HF.
S3 gallop
A major Framingham criterion for the diagnosis of HF.
Auscultation sounds: Third heart sound gallop
cardiomegaly
Cardiomegaly is a major Framingham criterion for the diagnosis of HF. Left ventricular dilation or hypertrophy are common findings.
hepatojugular reflux
A major Framingham criterion for the diagnosis of HF.
rales
A major Framingham criterion for the diagnosis of HF.
uncommon
orthopnea and paroxysmal nocturnal dyspnea
Orthopnea (dyspnea that develops in the recumbent position) usually 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.
nocturia
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
common
tachycardia (heart rate >120 beats per minute)
A minor Framingham criterion for the diagnosis of HF.
chest discomfort
A symptom of poor coronary perfusion.
hepatomegaly
A minor Framingham criterion for the diagnosis of HF; may cause abdominal discomfort/distension and nausea.
ankle edema
A minor Framingham criterion for the diagnosis of HF.
night cough
A minor Framingham criterion for the diagnosis of HF.
signs of pleural effusion
A minor Framingham criterion for the diagnosis of HF.
fatigue, muscle weakness, or tiredness
Symptom of poor tissue (muscle) perfusion.
uncommon
palpitations, presyncope, or syncope
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. Syncope may result from fast atrial arrhythmias or ventricular tachycardia, or rarely from significant valvular disease, e.g., aortic stenosis.
lethargy/confusion
Symptom of poor tissue (brain) perfusion.
Risk factors
strong
coronary artery disease (CAD)
myocardial infarction (MI)
hypertension
Hypertension is a common comorbidity and cause of HF. Presence of hypertension confers a 2- to 3-fold increase in risk of developing HF.[13][14][17][18][19][20][23] Elevated systolic blood pressure (BP), elevated diastolic BP, and elevated pulse pressure have all been associated with increased risk for HF.[24][25] Among the Framingham cohort, a 1 standard deviation (20 mmHg) increase in systolic BP was associated with a 56% increased risk for HF, a 1 standard deviation (10 mmHg) increase in diastolic BP was associated with 24% increased risk, and a 1 standard deviation (16 mmHg) increase in pulse pressure was associated with a 55% increase in risk.[24] A study in Japan found that higher nighttime BP and a riser pattern of nocturnal BP (nighttime BP higher than daytime BP) were significantly associated with the risk of total cardiovascular disease and HF.[26]
diabetes mellitus
Diabetes mellitus has been associated with a 3- to 5-fold increase in the risk of developing HF and is a common comorbidity.[14][17][18][20][27][28] The highest increase in relative risk is found among women and people with asymptomatic left ventricular dysfunction.[14][20][27] Even a slight increase of 1% in hemoglobin A1c has been linked to a greater than 10% risk of hospitalization for HF or death.[29] Both type 1 and type 2 diabetes increase the risk of developing HF across the entire range of glucose levels; however, HF may be more prevalent in people with type 1 compared with type 2 diabetes.[30]
dyslipidemia
Lipid abnormalities have been linked to increased risk for HF; they are common comorbidities.[31][32][33] 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 HF, and men with ratios of greater than 10 had a nearly 5-times greater incidence of HF.[31] In the same study, women with ratios greater than 10 had more than 6-times greater incidence of HF than women with ratios less than 5.[31] In one clinical trial of patients with coronary artery disease, lipid lowering was associated with a 21% reduction in the risk of developing HF.[34]
older age
Increasing age has been consistently linked to a higher risk of developing HF.[13][14][17][18][19][35][36] In the Framingham cohort, the incidence of HF increased steadily with increasing age.[14] 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.[18] In another study, the incidence rate of HF among the oldest people (age >80 years) was double that of the youngest people (age 65 to 69 years).[36]
male sex
Male sex has been consistently linked to a higher risk of developing HF, and HFrEF.[13][14][17][18][19][20][35][36][37] In the Framingham cohort, women had a one third lower incidence of HF than men and male sex was associated with a hazard ratio of 1.34.[14][18][20] In other studies the incidence among males is 2 to 4 times that of females.[13][36] 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 HF of 1.24.[16]
obesity
Obesity is a common comorbidity and excess body weight is an established risk factor for the development of HF.[38] Among a subset of the Framingham cohort, the risk of HF increased by 5% for men and 7% for women with each increase of 1 in body mass index; obese people (body mass index 30 or above) had a risk of HF double that of nonobese people.[39] Obesity may result in HF by inducing hemodynamic and myocardial changes that lead to cardiac dysfunction, or may predispose to HF risk factors (e.g., hypertension, obstructive sleep apnea) and other cardiovascular disease risk factors (e.g., diabetes, dyslipidemia).[40]
exposure to cardiotoxic agents
Doxorubicin and cyclophosphamide can cause myocardial damage leading to left ventricular dysfunction and HF.[41][42] These chemotherapeutic agents increase risk for HF both during acute treatment and for several months after treatment has ended, with risk increasing as cumulative dose increases.[43][44] In addition, trastuzumab, sunitinib, clofarabine, and carfilzomib have also been associated with the development of cardiomyopathy.[45] Anthracyclines have also been associated with an increased risk of congestive HF.[46]
Mediastinal irradiation can cause direct myocardial damage leading to left ventricular dysfunction and HF for several years after the treatment has ended.[47]
left ventricular dysfunction
Moderate-to-severe asymptomatic left ventricular dysfunction (ejection fraction [EF] <40%) has been associated with a hazard ratio of HF of 7.8, while mild asymptomatic left ventricular dysfunction (EF 40% to 50%) has been associated with a hazard ratio of 3.3.[48]
left ventricular hypertrophy
Left ventricular hypertrophy, such as in hypertrophic obstructive cardiomyopathy, on electrocardiogram has been associated with a higher risk of HF, with highest relative risk among younger people.[49]
renal insufficiency
Chronic kidney disease is a common comorbidity. Renal insufficiency, defined by elevated serum creatinine (over 1.50 mg/dL in men and 1.30 mg/dL in women) or reduced creatinine clearance (less than 60 mL/minute), has been linked to increased risk for development of HF. Compared with people with creatinine of less than 1.10 mg/dL, people with creatinine of 1.30 to 1.49 mg/dL had almost double the risk of developing congestive HF, those with creatinine of 1.50 to 1.69 mg/dL had almost triple the risk, and those with creatinine greater than 1.70 mg/dL had almost quadruple the risk.[50][51]
valvular heart disease
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.[52] 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.[53] Ventricular remodeling alters cardiac contractility and increases the risk of HF. Aortic stenosis, aortic regurgitation, mitral regurgitation, and tricuspid regurgitation are important comorbidities of HF.
sleep apnea
elevated homocysteine
In the Framingham cohort, elevated plasma homocysteine levels were linked with a roughly three-quarter increased risk for developing HF.[59]
family history of HF
Several polymorphisms have been linked with an increased risk of developing HF. 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 HF. A second polymorphism that was evaluated as a candidate for developing HF 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 HF.[63]
atrial fibrillation
Often coexists with HF, and the two conditions may cause or exacerbate each other.[9] Atrial fibrillation increases the risk of thrombo-embolic events (e.g., stroke) and may lead to a worsening of symptoms. Development of atrial fibrillation in patients with HF is associated with a worse prognosis; however, those who develop atrial fibrillation first (tachycardiomyopathy) may have a more favorable clinical course.[9][64]
thyroid disorders
anemia
Anemia is a strong risk factor and prognostic marker of poor survival. A high prevalence of iron deficiency has been reported in HF.[65] Iron deficiency in HF 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]
elevated tumor necrosis factor-alfa (TNF-alfa) and interleukin-6 (IL-6)
elevated C-reactive protein (CRP)
decreased insulin-like growth factor-1 (IGF-1)
IGF-1 has been shown to have positive inotropic effects and to decrease the rate of cellular apoptosis.[70][71] IGF-1 has also been tentatively linked to vasodilation, which may improve cardiac emptying.[72] Among the Framingham cohort, patients with a serum IGF-1 level below 140 mg/L had double the risk of developing HF.[73]
elevated natriuretic peptides
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 HF. BNP levels above the 80th percentile (20.0 picograms/mL for men and 23.3 picograms/mL for women) were associated with a 3-fold increase in HF risk.[74]
dilation of the left ventricle
The risk-factor-adjusted hazard ratio for HF 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.[48]
increased left ventricular mass
abnormal left ventricular diastolic filling
metabolic syndrome or cardiovascular-kidney-metabolic (CKM) syndrome
Metabolic syndrome is a cluster of common conditions, including insulin resistance, impaired glucose tolerance, abdominal obesity, reduced high-density lipoprotein-cholesterol levels, elevated triglycerides, and hypertension. Metabolic syndrome and the individual components are risk factors for development and progression of HF.[77] CKM syndrome is a disorder defined by the American Heart Association (AHA) to reflect the connections between metabolic disease (obesity, diabetes, metabolic syndrome), kidney disease, and cardiovascular disease (CVD).[78][79] It includes both individuals at risk for CVD (due to the presence of metabolic risk factors, CKD, or both) and individuals with existing CVD. Poor CKM health affects nearly all organ systems and is associated with cardiovascular morbidity and mortality. The AHA has proposed a CKM syndrome staging system based on patient risk factors and opportunities for prevention and care. The AHA recommends that these patients are managed by an interdisciplinary team with targeted referral of high-risk CKM patients to appropriate subspecialists.[78]
weak
low socioeconomic status
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 HF of 1.22 (population attributable risk 8.9%).[16]
tobacco consumption
alcohol misuse
Chronic excess alcohol consumption is a risk factor for development of HF.[83][84][85][86][87] This may be related to both direct myocardial toxicity of alcohol and the higher risk of hypertension development. The effect of moderate alcohol consumption on the risk of HF is uncertain, as studies have not demonstrated a causal relationship.
excess sodium 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.[88]
tachycardia
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 HF.[52]
depression/stress
microalbuminuria
Although no link between microalbuminuria and the development of HF has been established, microalbuminuria was linked with a 3-fold increased risk of HF hospitalization in the Heart Outcomes Prevention Evaluation study.[92]
aspirin use
In an individual patient data pooled analysis of six observational studies, aspirin use was associated with an increased risk of HF in people over 40 years old (mean age 67 years) with at least one of the following predisposing factors for HF: smoking, obesity, high blood pressure, high cholesterol, diabetes, cardiovascular disease.[93]
micronutrient deficiency
Deficiency of micronutrients, such as selenium, zinc, and copper, has been linked to the development of cardiomyopathy.[94]
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