Treat the cause and left ventricular hypertrophy regressed in 54.2% of patients
In short
Across 1,454 patients with primary aldosteronism (36 referral centres in Spain, Italy and Germany; mean age 51), baseline left ventricular hypertrophy prevalence was 49.4%. Among the 473 who had follow-up echocardiography after adrenalectomy or mineralocorticoid receptor antagonist therapy, LVH regressed in 54.2% over a median of 51 months — 61.9% after surgery versus 48.6% on medical therapy (p=0.043). Left ventricular mass index fell significantly after both, meaning pathologically thickened heart muscle is not fixed damage but a structure that shrinks once the load is removed. Higher pretreatment blood pressure and aldosterone made regression less likely.
Start with the numbers. Of 1,454 patients with primary aldosteronism (mean age 51, 58.7% male) pooled from 36 referral centres in Spain, Italy and Germany, 49.4% had left ventricular hypertrophy before treatment. Half. Among the 473 who had a follow-up echocardiogram, LVH had regressed in 54.2% after a median of 51 months.
Primary aldosteronism is secondary hypertension driven by excess aldosterone from the adrenal gland. The blood pressure is not itself the disease; something else is raising it. What this study asks is what happens to an already-thickened ventricle once that driver is taken away.
Why does thickened heart muscle thin out again?
Because thickening is an adaptation to load rather than a scar. While pressure load and aldosterone signalling persist, the heart keeps the wall thick; remove the stimulus and mass moves back down. The evidence here is that left ventricular mass index fell significantly in both arms — those who had the adrenal gland removed and those whose receptors were blocked pharmacologically.
This sits on the same axis as the finding that an athlete's enlarged heart and a diseased one differ at the molecular level, covered in how exercise-grown and diseased hearts differ.
So why did nearly half not regress?
What separated them was not the treatment but the state at which treatment started. Higher pretreatment blood pressure and higher aldosterone levels both predicted a lower chance of regression, and that held regardless of surgery or medication. Conversely, patients with complete biochemical success showed the largest reduction in left ventricular mass index.
There is a window for reversal, and it narrows the longer and harder the load runs. The meta-analysis putting LVH at 36.6% of hypertensive patients is in blood pressure and heart wall thickness; this cohort fills in what can happen afterwards.
What does this mean for a lifter?
People who lift heavy tend to read wall thickness as a product of training. This study points the other way: some of what thickens a ventricle is a treatable cause unrelated to training, and it is reversible. High blood pressure at a young age, pressure that stays high on multiple drugs, or hypertension alongside low potassium all belong to a category where looking for the cause is its own investigation.
- Check blood pressure as often as you check the log — lifting itself spikes pressure acutely, so what matters first is whether resting pressure is controlled.
- Uncontrolled hypertension is a diagnostic question — pressure that will not come down on added medication may be a cause problem rather than a dose problem.
- Later diagnosis means less reversal — the higher the pretreatment pressure and aldosterone, the lower the odds of regression.
- Training still belongs in the plan — the network meta-analysis showing every modality lowered blood pressure is in the exercise dose for blood pressure.
This is a retrospective cohort of patients diagnosed with primary aldosteronism, and it does not transfer directly to essential hypertension or to cardiac adaptation from training. If an ECG or echocardiogram has flagged left ventricular hypertrophy, that is clinical territory rather than something to self-assess.
Frequently asked questions
Can left ventricular hypertrophy be reversed?
In many patients, yes, once the cause is removed. Among 473 patients with primary aldosteronism followed for a median of 51 months after targeted treatment, LVH regressed in 54.2% and left ventricular mass index fell significantly.
What is primary aldosteronism?
It is secondary hypertension caused by excess aldosterone secretion from the adrenal gland. The blood pressure is a symptom of a separate driver, so treatment targets that driver — either adrenalectomy or a mineralocorticoid receptor antagonist.
Which reverses it better, surgery or medication?
In this cohort, regression occurred in 61.9% after adrenalectomy versus 48.6% on a mineralocorticoid receptor antagonist (p=0.043). Left ventricular mass index nonetheless fell significantly with both approaches.
Why do some patients not regress?
Higher pretreatment blood pressure and aldosterone levels were both associated with lower odds of regression, independently of treatment modality. Patients who achieved complete biochemical success showed the largest fall in left ventricular mass index.
Is an athlete's enlarged heart the same problem?
No. This study concerns pathological thickening driven by hormonal and pressure load, which arises through different mechanisms than cardiac adaptation to training. Distinguishing the two when an ECG or echocardiogram flags hypertrophy requires imaging read alongside clinical context.
Source: PubMed