Cardiology
Left Ventricular Hypertrophy
Myocardial thickening from chronic pressure or volume overload — and an independent risk multiplier
LVH is thickening of the LV wall from chronic load. LV mass index > 115 g/m² in men or > 95 g/m² in women is diagnostic. LVH doubles MI risk and is a major substrate for AF and ventricular arrhythmia.
- LVMI threshold (men)> 115 g/m²
- LVMI threshold (women)> 95 g/m²
- Top driverSystemic hypertension
- Pattern · pressure loadConcentric remodeling (RWT > 0.42)
- Pattern · volume loadEccentric remodeling (RWT ≤ 0.42)
- MI riskApproximately doubled, independent of HTN
Interactive visualization
Press play, or step through manually. Compare a normal LV wall with concentric and eccentric remodeling — and watch the LV mass calculation build.
Watch the 60-second explainer
A condensed visual walkthrough — narrated, captioned, under a minute.
What LVH actually is
Cardiac myocytes add sarcomeres in response to mechanical load. Pressure load — pumping against high systemic pressure or a narrowed aortic valve — drives parallel sarcomere addition, thickening the wall without changing chamber size (concentric remodeling). Volume load — chronic regurgitation or shunts — drives series sarcomere addition, dilating the chamber (eccentric remodeling). Both states are LVH, but they look and behave very differently.
Measuring LV mass
The clinical standard is echocardiography. From three measurements — interventricular septal thickness (IVSd), posterior wall thickness (PWd), and LV internal diameter at end-diastole (LVIDd) — the Devereux formula gives LV mass:
LV mass (g) = 0.8 × 1.04 × [(IVSd + LVIDd + PWd)³ − LVIDd³] + 0.6
Divide by body surface area to get LV mass index (LVMI). Diagnose LVH when LVMI exceeds 115 g/m² in men or 95 g/m² in women. Relative wall thickness (RWT = 2 × PWd / LVIDd) above 0.42 means concentric; below means eccentric. Cardiac MRI is the most accurate technique but is reserved for ambiguous cases or tissue characterization.
Worked clinical example
A 58-year-old man with 15 years of uncontrolled hypertension (typical home BP 158/96) comes for evaluation of exertional dyspnea. Echo measurements: IVSd 13 mm, PWd 13 mm, LVIDd 47 mm. Body surface area 1.96 m². Plug into Devereux:
- Sum cubed: (13 + 47 + 13)³ = 73³ = 389,017 mm³
- Subtract LVIDd cubed: 389,017 − 47³ = 389,017 − 103,823 = 285,194 mm³
- Multiply: 0.8 × 1.04 × 285,194 = 237,281 mm³ → ~237 g (convert mm³ of muscle to g by density factor implicit in 0.8 × 1.04)
- Index: 237 / 1.96 = 121 g/m² → LVH by criteria (> 115 in men)
- RWT: 2 × 13 / 47 = 0.55 → concentric pattern (consistent with pressure overload)
Plan: aggressive BP control to < 130/80, prioritize ACE inhibitor or ARB (most effective class for LV mass regression), assess for OSA, screen renal function, repeat echo at 1 year. With sustained control, LVMI typically falls 10-15% per year. A 1-standard-deviation reduction in LV mass tracks with about a 20% drop in cardiovascular events.
Concentric vs eccentric — the lookup table
| Feature | Concentric LVH | Eccentric LVH |
|---|---|---|
| Load type | Pressure overload | Volume overload |
| Common cause | Hypertension, aortic stenosis, HCM | MR, AR, DCM, severe anemia |
| Sarcomere addition | Parallel (thickens wall) | Series (elongates fiber) |
| Wall thickness | Increased | Normal or slightly increased |
| Chamber size | Normal or small | Dilated |
| Relative wall thickness (RWT) | > 0.42 | ≤ 0.42 |
| Ejection fraction | Preserved (HFpEF risk) | Often reduced (HFrEF risk) |
| Treatment focus | Reduce afterload (BP, valve replacement) | Reduce preload, fix regurgitation |
Common mistakes
- Calling athlete's heart pathologic. Endurance athletes show balanced concentric and eccentric features that regress with detraining; no excess events.
- Trusting ECG criteria too much. Sokolow-Lyon and Cornell are very specific but only 30-50% sensitive — a normal ECG does not rule out LVH on echo.
- Missing HCM in young patients. Wall thickness > 15 mm without obvious load, especially asymmetric septum, demands HCM workup including genetic testing.
- Treating LVH only when ECG-positive. The risk of MI and AF tracks with echo-measured mass, not ECG voltage.
- Choosing beta blockers as first-line for LV mass regression in HTN. ACE inhibitors and ARBs lead head-to-head trials; thiazides and calcium blockers are next; beta blockers lag.
Frequently asked questions
What causes LVH?
Pressure overload (hypertension is by far the most common, then aortic stenosis, hypertrophic cardiomyopathy, coarctation) drives concentric hypertrophy — walls thicken without chamber dilation. Volume overload (chronic mitral or aortic regurgitation, severe anemia, AV shunts, dilated cardiomyopathy) drives eccentric remodeling — chamber enlarges with relatively preserved wall thickness. Athlete's heart is a physiologic adaptation: balanced wall and chamber growth, often reversible with detraining, and not associated with adverse outcomes.
How is LVH diagnosed?
Echocardiogram is the standard. LV mass is calculated by the Devereux formula from interventricular septal thickness, posterior wall thickness, and LV internal diameter, then indexed to body surface area. Threshold: >115 g/m² in men, >95 g/m² in women. Relative wall thickness (2 × posterior wall / LV diameter) > 0.42 distinguishes concentric from eccentric patterns. Cardiac MRI provides superior accuracy and tissue characterization. ECG criteria (Sokolow-Lyon: S in V1 + R in V5/V6 > 35 mm; Cornell: R in aVL + S in V3 > 28 in men or 20 in women) are specific but insensitive.
Why is LVH dangerous?
Hypertrophied myocardium has increased oxygen demand without proportional increase in capillary supply, predisposing to subendocardial ischemia. It is electrically heterogeneous, creating substrate for both atrial fibrillation and ventricular arrhythmia. It is fibrotic, impairing diastolic filling and causing HFpEF. Independent of risk factors, LVH approximately doubles the risk of myocardial infarction, stroke, and incident heart failure, and increases sudden cardiac death risk roughly threefold.
Can LVH be reversed?
Yes. Aggressive treatment of the underlying cause regresses LV mass over months to years. For hypertensive LVH, ACE inhibitors and ARBs are the most effective antihypertensive class at reducing LV mass, somewhat ahead of calcium channel blockers and well ahead of beta blockers (in head-to-head trials). Aortic valve replacement reverses LVH from aortic stenosis substantially within 1 year. Regression correlates with reduced cardiovascular events — about a 20% reduction in major events per standard deviation drop in LV mass.
Concentric vs eccentric — why does the pattern matter?
Concentric hypertrophy (thick walls, normal or small chamber, relative wall thickness > 0.42) typically reflects pressure overload — hypertension, aortic stenosis — and presents with diastolic dysfunction; ejection fraction is preserved but the chamber cannot fill. Eccentric hypertrophy (chamber dilated, wall thickness preserved relative to volume, RWT ≤ 0.42) reflects volume overload — mitral or aortic regurgitation, dilated cardiomyopathy — and tracks with systolic dysfunction (reduced ejection fraction). Treatment differs: pressure relief for concentric, volume relief or valve repair for eccentric.
How does LVH relate to arrhythmia risk?
Multiple mechanisms. Atrial dilation from raised LV filling pressures provides AF substrate — LVH is a major upstream cause of AF. Ventricular fibrosis and dispersion of repolarization in hypertrophied muscle create re-entry circuits for ventricular arrhythmia. Subendocardial ischemia in thick poorly perfused walls triggers ectopy. Patients with LVH and unexplained syncope or ventricular ectopy deserve evaluation for inherited cardiomyopathy (HCM) and may need ICD consideration if other risk markers are present.
When should you suspect hypertrophic cardiomyopathy?
Wall thickness > 15 mm without an obvious load (no severe hypertension, no aortic stenosis), particularly with asymmetric septal hypertrophy or systolic anterior motion of the mitral valve, suggests hypertrophic cardiomyopathy (HCM). Family history, unexplained syncope on exertion, or wall thickness > 30 mm in a young person are classic features. HCM is the most common monogenic cardiac disease (~1 in 500), most often from MYH7 or MYBPC3 mutations. Genetic testing and family screening are indicated when suspected.