Systolic vs. Diastolic Heart Failure

Heart failure is not a single disease — it is a clinical syndrome that can arise from very different underlying problems with how the heart functions. The distinction between systolic and diastolic heart failure (now more precisely called heart failure with reduced ejection fraction and heart failure with preserved ejection fraction) is fundamental to understanding the condition, because these two types have different causes, different pathophysiology, and respond to different treatments.

The Cardiac Cycle: Systole And Diastole

To understand systolic vs. diastolic heart failure, it helps to understand the two phases of each heartbeat:

Systole: The contraction phase. The ventricles contract, generating pressure that ejects blood into the aorta (from the left ventricle) and pulmonary artery (from the right ventricle). Normal systolic function = adequate contractile strength.

Diastole: The relaxation and filling phase. After contraction, the ventricles relax and fill with blood from the atria. Normal diastolic function = the ventricle relaxes fully and fills adequately at normal pressures.

Both phases are essential to effective cardiac performance. Either can be disrupted in heart failure.

SYSTOLIC HEART FAILURE (HFrEF — HEART FAILURE WITH REDUCED EJECTION FRACTION)

Systolic heart failure occurs when the ventricle's contractile function is impaired — the heart cannot generate adequate force to eject blood normally. The ejection fraction (EF) — the proportion of blood in the ventricle that is ejected with each beat — falls below 40% (normal is 55–70%).

Pathophysiology: The left ventricle typically dilates (enlarges) as it attempts to compensate for reduced contractile function. A larger chamber can accommodate more blood and, by increasing stroke volume (the amount of blood ejected), partially compensate for lower ejection fraction. This dilation and remodeling progressively worsens function over time.

Common causes of HFrEF:

• Prior myocardial infarction (heart attack): Scar tissue replaces functioning muscle, directly reducing contractile mass
• Dilated cardiomyopathy: Enlargement and weakening of the ventricle from various causes (genetic, alcohol, chemotherapy, viral infection, idiopathic)
• Longstanding hypertension: Eventually the chronically overloaded heart dilates and fails
• Valvular heart disease (aortic regurgitation, mitral regurgitation): Volume overloading the left ventricle

Who gets HFrEF: More common in men; more often associated with coronary artery disease and prior heart attack; tends to occur at younger ages than HFpEF.

DIASTOLIC HEART FAILURE (HFpEF — HEART FAILURE WITH PRESERVED EJECTION FRACTION)

Diastolic heart failure occurs when the ventricle's contractile function is normal or near-normal (EF ≥ 50%), but the ventricle is stiff and cannot relax and fill properly. Because the ventricle cannot fill to its normal volume at normal pressures, blood backs up — elevated filling pressures transmit back to the lungs, causing congestion.

Think of it this way: A normal heart is like a flexible rubber ball — it contracts forcefully and relaxes to refill easily. A diastolic heart failure heart is like a tennis ball — it can still squeeze (contract normally), but it is stiff and doesn't expand easily to fill.

Pathophysiology: The left ventricular wall is hypertrophied (thickened) and stiff. Elevated filling pressures cause congestion of the pulmonary veins and lungs, producing the same symptoms as systolic heart failure (shortness of breath, reduced exercise tolerance) — but with preserved contractile function.

Common causes of HFpEF:

• Hypertension: The most common cause — chronically elevated blood pressure causes concentric hypertrophy (thickening of the ventricular wall) without dilation
• Obesity: Directly contributes to diastolic dysfunction through multiple mechanisms
• Diabetes: Diabetic cardiomyopathy involves diastolic dysfunction
• Aging: The heart naturally becomes stiffer with age — diastolic dysfunction is very common in elderly adults
• Hypertrophic cardiomyopathy (HCM): Genetic condition causing abnormal hypertrophy
• Infiltrative diseases (amyloidosis): Protein infiltration makes the myocardium extremely stiff

Who gets HFpEF: More common in women; older patients; those with hypertension, obesity, and diabetes. HFpEF is now the predominant type of heart failure — approximately 50% or more of all heart failure patients.

How They Present Similarly

Both types of heart failure produce identical symptoms — shortness of breath (with exertion, lying flat, or at rest), leg swelling, fatigue, and reduced exercise tolerance. Distinguishing them requires:

Echocardiography: The primary diagnostic tool. An echocardiogram directly measures ejection fraction and also assesses ventricular size, wall thickness, and diastolic filling patterns. HFrEF shows a dilated, poorly contracting ventricle with low EF; HFpEF shows a normal-sized or slightly enlarged ventricle with thickened walls, normal or near-normal EF, and elevated filling pressures on Doppler assessment.

BNP/NT-proBNP blood tests: Biomarkers released by the heart under stress — elevated in both types of heart failure; very helpful in confirming the diagnosis and assessing severity.

Why The Distinction Matters: Different Treatments

This is where the distinction between HFrEF and HFpEF becomes clinically critical:

For HFrEF, multiple drug classes have been proven to reduce mortality:

• ACE inhibitors/ARBs (lisinopril, sacubitril-valsartan)
• Beta-blockers (carvedilol, metoprolol succinate, bisoprolol)
• Mineralocorticoid receptor antagonists (spironolactone, eplerenone)
• SGLT2 inhibitors (dapagliflozin, empagliflozin — newer but now guideline-recommended)

For HFpEF, treatments are more limited — fewer medications have shown clear mortality benefits:

• SGLT2 inhibitors (dapagliflozin, empagliflozin — the most recently established treatments for HFpEF)
• Spironolactone (modest evidence)
• GLP-1 receptor agonists (semaglutide — showing promise for HFpEF related to obesity)
• Diuretics for symptom control (reduce congestion)
• Aggressive management of underlying conditions (blood pressure, obesity, diabetes, AFib)

The limited pharmacological options for HFpEF partly explain why it carries a similar prognosis to HFrEF despite preserved ejection fraction.