Diastolic dysfunction (DD) is a common heart condition where the main pumping chambers, the ventricles, become stiff and struggle to relax fully after contracting. This stiffness prevents the heart from efficiently filling with blood during the resting phase of the heartbeat, known as diastole. When the heart cannot fill properly, pressure builds up inside the chamber and backs up into the lungs and other parts of the body, leading to symptoms like shortness of breath and fluid retention.
When this condition leads to symptoms of heart failure while the heart’s pumping function (ejection fraction) remains normal, it is classified as heart failure with preserved ejection fraction (HFpEF). Medication management for diastolic dysfunction is complex and aims to manage symptoms and address the underlying disease process. A personalized treatment plan is necessary because the approach involves balancing symptom relief with long-term heart protection.
Symptom Management: Addressing Fluid Retention
Fluid accumulation and congestion, leading to symptoms like ankle swelling and shortness of breath, are the most common issues in diastolic dysfunction. Medications known as diuretics, or “water pills,” are the primary treatment for managing this fluid overload. These agents help the body excrete excess salt and water through the kidneys, which reduces the overall volume of fluid circulating in the bloodstream and lungs.
Loop diuretics, such as furosemide, torsemide, and bumetanide, are frequently used because they are highly effective at promoting rapid and substantial fluid loss by acting on the loop of Henle in the kidney. Thiazide diuretics, including hydrochlorothiazide and chlorthalidone, work further down the kidney tubule and are sometimes used alone or in combination with loop diuretics for additional effect. While diuretics offer immediate symptom relief by lowering the filling pressure in the heart, their dosing must be carefully monitored. Using too high a dose can lead to dehydration and dangerously low blood pressure, which can impair the heart’s ability to pump effectively.
Improving Cardiac Relaxation and Rate Control
A core problem in diastolic dysfunction is the stiff, slow-to-relax ventricle, which needs more time to fill with blood. Medications that slow the heart rate can extend the diastolic filling period, allowing the ventricle more time to relax and accept a normal volume of blood before the next contraction. Beta-blockers, such as metoprolol or carvedilol, are commonly used to achieve this controlled reduction in heart rate.
Slowing the heart rate with beta-blockers improves the efficiency of filling and helps prevent the rapid pressure increases that occur during exercise or stress. Certain non-dihydropyridine calcium channel blockers, including verapamil and diltiazem, are also beneficial because they directly enhance the relaxation properties of the heart muscle cells. These agents reduce the movement of calcium into the muscle cell, which facilitates better and faster relaxation during diastole.
Modifying Disease Progression (Long-Term Therapies)
The most significant recent advancements in treating heart failure with preserved ejection fraction (HFpEF) involve medications that modify the long-term course of the disease. Sodium-glucose cotransporter-2 (SGLT2) inhibitors, originally developed for diabetes, have emerged as foundational therapy for HFpEF because they reduce the risk of heart failure hospitalizations. These drugs, such as empagliflozin and dapagliflozin, work through mechanisms beyond blood sugar control, including reducing fluid retention, improving kidney function, and exerting direct anti-inflammatory effects on the heart.
Another group of medications targets the body’s neurohormonal systems, particularly the renin-angiotensin-aldosterone system (RAAS), which contributes to heart stiffness and damage over time. Angiotensin-converting enzyme (ACE) inhibitors (e.g., lisinopril) and Angiotensin Receptor Blockers (ARBs) (e.g., valsartan) block the effects of hormones that cause blood vessel constriction and cardiac tissue scarring. By reducing systemic vascular resistance and blocking these detrimental pathways, they help prevent the progressive fibrosis and remodeling of the heart muscle characteristic of diastolic dysfunction.
Mineralocorticoid Receptor Antagonists (MRAs), such as spironolactone and eplerenone, are also part of this long-term strategy. These medications block the effects of aldosterone, a hormone that promotes salt retention and contributes to fibrosis in the heart. By mitigating this scarring process, MRAs help preserve the heart’s ability to relax and fill over many years, offering a sustained benefit against disease progression.
Medications for Associated Underlying Conditions
Diastolic dysfunction often develops as a consequence of other long-standing health issues. Treating these underlying conditions is a necessary part of managing the heart problem. Hypertension, or high blood pressure, is one of the most common causes, as high pressure forces the heart muscle to work harder, leading to stiffening. Achieving strict blood pressure control is a primary goal, often using ACE inhibitors, ARBs, or calcium channel blockers, which directly address the pressure load on the heart.
Diabetes is another major contributor to diastolic dysfunction, and certain anti-diabetic medications offer unique cardiovascular protection. Glucagon-Like Peptide-1 Receptor Agonists (GLP-1 RAs), such as liraglutide, have been shown to improve diastolic function and reduce cardiovascular risk in patients with type 2 diabetes. These agents help reduce cardiac strain and improve the heart’s relaxation characteristics, offering a dual benefit for metabolic and cardiac health.
Atrial fibrillation (A-fib) frequently co-exists with diastolic dysfunction and significantly worsens symptoms because the rapid, irregular heart rhythm does not allow enough time for the stiff ventricle to fill. Medications like beta-blockers and certain calcium channel blockers are used to control the ventricular rate, ensuring the heart beats slowly enough to maximize filling time. Antiarrhythmic drugs may also be used to restore a normal heart rhythm, which is important for maintaining optimal cardiac output.