Hypertensive heart disease

Cardiac changes caused by chronic high blood pressure, primarily pressure-overload–induced concentric left ventricular hypertrophy (LVH) leading to reduced ventricular compliance. This remodeling results in a stiff left ventricle with impaired diastolic filling and can progress to heart failure (typically HFpEF) and arrhythmias.

• Hypertension is extremely common and a major cause of heart disease worldwide. Long-standing high BP causes LVH that markedly increases the risk of heart failure (it accounts for ~25–50% of HF cases overall and up to 68% in the elderly). Hypertensive LVH also predisposes to atrial fibrillation and other arrhythmias, and is associated with higher rates of myocardial infarction and sudden cardiac death. Early recognition and treatment can prevent progression, and exam questions frequently test the signs (e.g., LVH on ECG, S4 gallop) and complications of hypertensive heart disease.

• Often asymptomatic early on: patients with chronic hypertension may have LVH for years with no overt symptoms (e.g., LVH noted incidentally on an ECG or echo).
• Progressive exertional dyspnea and decreased exercise tolerance as diastolic heart failure (HFpEF) develops (stiff LV cannot fill adequately). Patients may report fatigue or mild swelling; acute pulmonary edema can occur with blood pressure surges ("flash" pulmonary edema).
• New-onset atrial fibrillation (palpitations, irregularly irregular pulse) or other arrhythmias can be the first presentation, due to left atrial enlargement from long-standing LV stiffness. Some patients also experience angina or chest tightness (hypertrophied myocardium has increased oxygen demand, and coronary perfusion is relatively reduced).
• Physical exam may reveal a sustained apical impulse (LV heave) and a loud S4 gallop (atrial kick against a non-compliant LV). Signs of chronic hypertension (e.g., retinal changes) or heart failure (pulmonary rales, peripheral edema) may be present in advanced disease.

1. Suspect HHD in patients with long-standing hypertension and evidence of LVH (e.g., high-voltage QRS on ECG or an S4 heart sound). The best initial test is a transthoracic echocardiogram to assess LV wall thickness, mass, and diastolic function.
2. Electrocardiogram (ECG): may show LVH criteria (e.g., very tall S in V1 + R in V5 >35 mm) and a characteristic "strain" pattern (lateral ST depression and T-wave inversion) reflecting subendocardial ischemia. Chest X-ray is often normal until late (LVH doesn't greatly enlarge the silhouette unless accompanied by dilation).
3. Cardiac MRI: indicated if further characterization is needed – it precisely measures LV mass and can detect fibrosis. CMR can help distinguish hypertensive LVH from other causes (e.g., genetic hypertrophic cardiomyopathy or infiltrative disease).
4. Evaluate for other causes of LV hypertrophy in suspected HHD: check for aortic stenosis (murmur and valve calcification on imaging), review athletic history for athlete’s heart (physiologic hypertrophy), and consider genetic testing/family history if HCM is suspected. Typically, hypertensive LVH is concentric and diffuse, whereas HCM often shows asymmetric septal hypertrophy.

1. Aggressive blood pressure control is the cornerstone: target <130/80 mmHg if tolerated. Use ACE inhibitors or ARBs (which can promote LVH regression via RAAS blockade), often combined with thiazide diuretics or calcium channel blockers for optimal BP control.
2. Encourage lifestyle modifications: low-salt diet, weight loss, exercise, and avoiding excessive alcohol – these help improve blood pressure and reduce cardiac workload.
3. If diastolic heart failure (HFpEF) is present, manage volume overload with cautious diuretics (to relieve congestion without dropping BP too much). Control heart rate (beta-blockers or non-dihydropyridine CCBs) especially if atrial fibrillation is present, and consider anticoagulation for AF to prevent stroke.
4. In patients with advanced disease, follow heart failure guidelines: e.g., consider mineralocorticoid receptor antagonists or SGLT2 inhibitors which have shown benefit in HFpEF, and manage coronary artery disease risk factors aggressively. Importantly, regression of LVH is possible with sustained BP control, which improves outcomes.

• Mnemonic: Pressure overload (e.g., HTN, aortic stenosis) causes concentric hypertrophy; Volume overload (e.g., regurgitant valves, endurance training) causes eccentric hypertrophy. (Pressure → parallel sarcomere addition, walls thicken; Volume → series addition, chamber dilates.)
• Remember the heart sound: a stiff LV from LVH often produces an S4 ("atrial gallop") – a low-frequency sound just before S1, from the left atrium forcefully filling a non-compliant ventricle (common in hypertensive heart disease).
• ECG LVH criteria: One common board formula is S(V1) + R(V5 or V6) > 35 mm = LVH. Also look for the "LV strain" pattern (inverted T waves in V5-6, I, aVL) in a hypertensive patient – a clue to long-standing LVH.

• Long-time hypertensive patient with new atrial fibrillation (palpitations, dizziness) and rapid heart rate — can precipitate acute decompensated heart failure; requires prompt rate/rhythm control and anticoagulation.
• Flash pulmonary edema (acute onset severe dyspnea, pink frothy sputum) in a hypertensive patient — often due to sudden diastolic failure; treat as hypertensive emergency (IV nitroglycerin, diuretics) and ICU monitoring.
• Severe hypertensive emergency (BP >180/120 mmHg with chest pain, neurologic symptoms, or pulmonary edema) — immediate blood pressure reduction is critical to prevent acute heart failure, stroke, or myocardial infarction.

1. Uncontrolled hypertension with possible LVH (e.g., high BP readings, S4 gallop, ECG voltage) → Obtain an echocardiogram to assess for concentric LVH and diastolic function.
2. If echo shows concentric LVH with preserved EF (and no alternate cause) → Diagnose hypertensive heart disease (asymptomatic stage = HF stage B).
3. Begin intensive BP management: lifestyle changes + medications (often ACEi/ARB-based regimen) to reach goal BP; schedule follow-up to monitor BP and any symptoms.
4. If patient develops HFpEF symptoms (HF stage C) → add diuretics for symptom relief, manage atrial fibrillation if present (rate control, anticoagulation), and consider referral to cardiology for advanced therapies (e.g., SGLT2 inhibitors for HFpEF).
5. Follow-up: periodic echocardiography to track LVH regression or progression; ensure continued blood pressure control and monitor for complications (arrhythmias, ischemic events).

• Older adult with a history of poorly controlled hypertension, now with dyspnea on exertion, a loud S4 heart sound, and echo showing thickened LV walls but normal EF → Hypertensive heart disease (concentric LVH causing diastolic HF).
• Patient with chronic hypertension experiences sudden acute pulmonary edema (flash pulmonary edema) after a blood pressure surge; echo reveals concentric LV hypertrophy and diastolic dysfunction → acute decompensated hypertensive heart failure (HFpEF exacerbation from HHD).