Enlarged Heart: Causes, Diagnosis, Risk — and When an Athlete's Heart Is Normal

Key Takeaways: Enlarged Heart

In this article, an enlarged heart (cardiomegaly) is treated as a finding rather than a diagnosis in itself, and its cause needs to be established separately; left ventricular hypertrophy (thickened walls) and chamber dilatation are distinct structural findings, with causes ranging from high blood pressure to athletic training.
On a chest X-ray, a cardiothoracic ratio above 0.5 is the usual cut-off for cardiomegaly. In 79 hospital patients, X-ray identified 54.35% of the hearts that echocardiography showed to be enlarged, with a specificity of 90.90%.[1]
In 3220 Framingham adults aged 40 or over without clinically apparent cardiovascular disease, higher left ventricular mass on echocardiography predicted cardiovascular events and death, independently of blood pressure, other risk factors and ECG findings.[2]
Left ventricular hypertrophy was found in 36–41% of hypertensive patients across 30 studies, and in 56.0% of obese individuals across 22 studies.[3][4]
A normal ECG does not rule out left ventricular hypertrophy: in hypertensive patients, median ECG sensitivity ranged from 10.5% to 21% depending on the criterion used.[5]
In hypertension, regression of left ventricular hypertrophy (or persistently normal left ventricular mass) was associated with fewer cardiovascular events (adjusted hazard ratio 0.54) than persistent or new hypertrophy.[6]
In athletes, a large heart is often physiological: 14% of 1309 elite athletes had a left ventricular cavity of 60 mm or more with normal systolic function, while a wall thickness of 13 mm or more was found in only 1.7% of 947 elite athletes.[7][8]
After long-term detraining, wall thickness returned to normal in all 40 elite athletes studied, but substantial cavity dilatation persisted in 22%.[9]
In my clinical experience, an enlarged heart is often an incidental chest X-ray finding that turns out to be left ventricular hypertrophy from untreated hypertension, whereas athletes I see with a large heart tend to have a slow heart rate and normal or low blood pressure; when there are signs of heart failure, I see a cardiologist’s echocardiogram as the primary further investigation.

Introduction: Enlarged Heart

“Your heart looks enlarged” is a phrase that understandably worries people. It may come from a chest X-ray report, an ECG printout or an echocardiogram, and it is often delivered without much explanation. The finding is not a single disease. It is a description of size, and the important questions are what is enlarged, by how much, why, and whether the heart still works normally.

That distinction matters because the same finding can mean very different things. In adults aged 40 or older, higher left ventricular mass has been linked to higher cardiovascular risk.[2] In selected elite athletes, a large left ventricle with normal function has been interpreted as a training adaptation.[7] And in some young athletes, a thickened heart reflects hypertrophic cardiomyopathy, the most common cardiovascular cause of sudden death reported in one large US registry covering 1980–2006.[10]

As a physician and former competitive athlete, I see both sides of this question. This article covers what an enlarged heart means, its main causes, how it is measured, why it matters for long-term risk, whether it can return to normal, and how an athlete’s heart differs from a diseased one.

In my clinical experience, an enlarged heart is a fairly common finding, both at the health centre and in occupational health care, although I come across it somewhat more often in the former. Often it is a purely incidental finding on a chest X-ray taken for another reason. In other cases, the suspicion has already arisen earlier, for example because of a high blood pressure reading or because the ECG meets the voltage criteria for left ventricular hypertrophy. When they hear the term, some patients ask whether a bigger heart is not simply a good thing. In my view, it usually is not in this setting, and I explain that it is a different matter from an athlete’s enlarged heart.

What Does “Enlarged Heart” Actually Mean?

Two important structural findings associated with an enlarged heart are hypertrophy and chamber dilatation. The heart muscle wall can thicken, which is called hypertrophy, or a chamber can widen, which is called dilatation. These are distinct findings with different causes and implications, and an enlarged heart shadow on X-ray does not necessarily establish either finding. Dilated cardiomyopathy, for example, is defined by a dilated left ventricle together with reduced contractile function.[11]

On a standard chest X-ray, heart size is usually estimated with the cardiothoracic ratio: the width of the heart shadow divided by the width of the chest. A ratio above 0.5 on a posterior-anterior film is conventionally read as cardiomegaly.[1] The X-ray is easy to perform and cost-effective, but it is an indirect measure.[1] In a study of 79 hospital inpatients published in 2023, 28 (35.44%) had cardiomegaly on chest X-ray, whereas echocardiography identified 46 (58.22%).[1] The X-ray’s sensitivity was 54.35% and its specificity 90.90%, for an overall accuracy of 69.62%.[1]

In other words, a large heart shadow on X-ray usually corresponded to enlargement on echocardiography in this population, but a normal-looking shadow missed many enlarged hearts. The authors also noted that a normal heart size on X-ray does not guarantee normal heart function.[1] The study was small and limited to inpatients, so the figures may differ in other settings.

From a clinical perspective, the chest X-ray measurement itself is simple: the width of the heart is compared with the width of the chest. In medical school, at least, we were taught as a rule of thumb that if the heart covers more than half of the chest width, it may be a sign of an enlarged heart. In athletes, the situation is different, as discussed below.

Causes of an Enlarged Heart

High blood pressure

Left ventricular hypertrophy is described as a cardinal manifestation of hypertensive organ damage and is associated with increased cardiovascular risk.[3] A review of 30 echocardiographic studies published between 2000 and 2010, covering 37,700 treated and untreated hypertensive patients, found left ventricular hypertrophy in 36% of patients using conservative criteria and 41% using less conservative criteria.[3] The studies used 23 different definitions of hypertrophy, and eccentric hypertrophy was more common than the concentric form.[3] The signs of high blood pressure are covered separately.

In my patients, a large heart most often turns out to be left ventricular hypertrophy, and in my experience it is usually caused by untreated hypertension. It tends to appear in somewhat older patients whose blood pressure may have been raised for a long time. For some of them, it comes as a surprise that their blood pressure is high at all, and I then explain to them where the finding comes from.

Obesity

Excess body weight is also associated with left ventricular hypertrophy. A meta-analysis of 22 studies including 5486 obese individuals found left ventricular hypertrophy in 56.0% overall, with a range of 20.0–85.0% depending on the study and definition.[4] In the 15 studies that included non-obese controls, obese individuals had markedly higher odds of hypertrophy (odds ratio 4.19, 95% CI 2.67–6.53), and in a meta-regression, body mass index was positively associated with left ventricular mass.[4] Among obese patients with hypertrophy in the studies reporting geometry, the eccentric pattern was more common than the concentric one (66% versus 34%).[4]

Heart muscle disease

Cardiomyopathies are diseases of the heart muscle itself. In dilated cardiomyopathy, the left ventricle is enlarged and pumps less effectively.[11] Hypertrophic cardiomyopathy, in which the heart wall is abnormally thick, is discussed below in the athlete section, because separating it from a trained heart can be difficult.[8]

Patients with cardiomyopathy are less common, but not so rare that I would never see them. From time to time, such a patient comes to my clinic with a markedly enlarged heart on the chest X-ray, and the ECG may also look quite unusual. In my experience, these patients are referred to, and end up in, cardiology care very quickly, and their treatment is highly specialised. In my clinical experience, an inherited predisposition that runs in the family is not uncommon among them. I also occasionally see patients with a relative who has been diagnosed with an inherited cardiomyopathy, and they may need a referral for further investigation.

Why Heart Size Matters: Left Ventricular Mass and Risk

The Framingham Heart Study gave some of the clearest evidence that left ventricular mass measured by echocardiography carries prognostic information. Researchers measured left ventricular mass by echocardiography in 3220 adults aged 40 or older who had no clinically apparent cardiovascular disease, and followed them for four years.[2] During that time there were 208 new cardiovascular events, 37 cardiovascular deaths and 124 deaths from any cause.[2]

Left ventricular mass was associated with every outcome, and the association held after adjustment for age, diastolic blood pressure, pulse pressure, hypertension treatment, smoking, diabetes, obesity, cholesterol ratio and ECG evidence of hypertrophy.[2] For each 50 g per metre increase in left ventricular mass corrected for height, the adjusted relative risk of cardiovascular disease was 1.49 in men and 1.57 in women.[2] The corresponding relative risks were 1.73 and 2.12 for cardiovascular death, and 1.49 and 2.01 for death from any cause.[2]

These participants had no clinically apparent cardiovascular disease at the start, and echocardiographic mass added information beyond the traditional risk factors.[2] This is an observational association; it does not by itself show that the extra mass causes the events.

How an Enlarged Heart Is Diagnosed

A chest X-ray has limited sensitivity for cardiomegaly, as described above.[1]

ECG

The ECG can give indirect clues to left ventricular hypertrophy, mainly through QRS voltage criteria. A systematic review of 21 studies with 5608 hypertensive patients compared six widely used ECG criteria with echocardiography.[5] Median sensitivity was low, ranging from 10.5% for the Gubner index to 21% for the Sokolow-Lyon index, while median specificity ranged from 89% to 99%.[5] In primary care, a negative ECG using the Romhilt-Estes score would lower a typical pre-test probability of hypertrophy only from 33% to 31%.[5] The authors concluded that ECG criteria should not be used to rule out left ventricular hypertrophy in hypertensive patients.[5]

In my clinical experience, when the ECG does point towards an enlarged heart, it may show the voltage criteria for left ventricular hypertrophy, and sometimes also an increased P-terminal force or strain-type changes. These findings can raise the suspicion, but as the review above shows, a normal ECG does not exclude hypertrophy.

Echocardiography

In the chest X-ray study above, echocardiography was used as the gold standard for heart size.[1] Function also matters: in a large athlete study discussed below, the absence of systolic dysfunction was the basis for interpreting marked cavity dilatation as most likely physiological.[7] How blood markers such as NT-proBNP behave in trained individuals is covered in NT-proBNP in athletes.

When There Are Signs of Heart Failure

From a clinical perspective, a markedly enlarged heart may warrant a more comprehensive work-up. In my practice, I usually start with electrolytes, and a blood count and an ECG are also part of the assessment. Some patients may already have signs of heart failure, depending, for example, on whether there is swelling in the legs or shortness of breath. In my experience, the chest X-ray often already shows increased pulmonary congestion, and in some patients there may also be pleural fluid related to heart failure. Such a patient may be breathless and fluid-overloaded, with swelling and weight that may have increased gradually.

In my emergency work, I see these patients from time to time. In the acute situation, the fluid overload may need to be relieved on a ward. In my experience, furosemide is often used, and when it is given intravenously, the patient is usually admitted. Metolazone (Zaroxolyn) is sometimes needed as well, and the patient’s weight then usually falls considerably; combined diuretic treatment of this kind requires close monitoring of electrolytes and kidney function. In the wards where I have worked, patients are typically weighed daily, and fluid intake is assessed individually, with a fluid restriction in some patients.

These patients are then usually referred for cardiology assessment. In my view, a cardiology consultation is generally warranted at least once, in which the heart is examined with echocardiography. The echocardiogram also shows the ejection fraction, which is part of the heart failure assessment. In my experience, it can also be useful to test NT-proBNP in these patients, as it may point towards heart failure on a laboratory basis. Ultimately, however, I see echocardiography performed by a cardiologist as the primary further investigation, in addition to the chest X-ray.

Can an Enlarged Heart Go Back to Normal?

In some situations, yes. In hypertension, a meta-analysis identified five studies including 3149 patients and pooled data from 2449 of them.[6] Compared with persistent or newly developed left ventricular hypertrophy, regression of hypertrophy or persistently normal left ventricular mass was associated with fewer cardiovascular events (adjusted hazard ratio 0.54, 95% CI 0.35–0.84).[6] The authors noted that further research is needed to establish whether regression benefits all hypertensive patients and ethnic groups.[6] How lifestyle measures and medication affect blood pressure itself is reviewed in how to lower blood pressure.

In selected athletes, a substantial reduction in training reduced heart dimensions, although cavity enlargement did not always return to normal, as described in the next section.[12][9]

Enlarged Heart in Athletes: Athlete’s Heart or Disease?

How large can a healthy athlete’s heart become?

Intensive, long-term athletic conditioning has been associated with left ventricular cavity enlargement, which in a large study of elite athletes was considered most likely an extreme physiological adaptation when systolic function was normal.[7] How training affects stroke volume and resting heart rate is covered separately, as are typical ranges for a normal heart rate.

In 1309 elite athletes (957 men and 352 women) from 38 sports, left ventricular end-diastolic cavity size ranged from 38 to 66 mm in women and from 43 to 70 mm in men.[7] Most athletes (55%) had a cavity of 54 mm or less, but 185 (14%) had a substantially enlarged cavity using an arbitrary clinical cut-point of 60 mm, a degree of enlargement compatible with dilated cardiomyopathy, although cavity size alone does not establish that diagnosis.[7] These athletes had normal systolic function, no regional wall-motion abnormalities, and remained free of cardiac symptoms over 1 to 12 years of follow-up (mean 4.7 years).[7] Larger body surface area and endurance sports such as cycling, cross-country skiing and canoeing were the main determinants, and the authors noted that the long-term significance of such enlargement was not known.[7]

Wall thickness is a different matter. Among 947 elite athletes, the thickest left ventricular wall measured 16 mm, and only 16 athletes (1.7%) had a wall of 13 mm or more — 15 rowers or canoeists and one cyclist, with none among 728 athletes from 22 other sports.[8] Every athlete with a wall of 13 mm or more also had an enlarged cavity (55–63 mm).[8] In this study, the authors concluded that a wall thicker than 16 mm with a non-dilated cavity in an athlete is likely to represent pathological hypertrophy such as hypertrophic cardiomyopathy.[8] This 16 mm figure comes from a 1991 cohort and is not a diagnostic cut-off: current European guidelines define hypertrophic cardiomyopathy as increased left ventricular wall thickness or mass that is not solely explained by abnormal loading conditions.[13]

In my view, an athlete’s enlarged heart differs from hypertensive left ventricular hypertrophy partly because the stimulus behind it is so different. In my understanding, in hypertensive hypertrophy it is mostly the left ventricle that enlarges; the right ventricle may also be affected, but the change is predominantly left-sided. In athletes, by contrast, the enlargement is more physiological and the hypertrophy is more even. Athletes often have a larger stroke volume and a low heart rate, and on auscultation I may hear a very slow heart rate. When I then measure their blood pressure, in the athletes I see it is often low or normal. In patients with left ventricular hypertrophy, on the other hand, office blood pressure is in my experience usually clearly raised, although this depends somewhat on the situation, and home readings may be lower.

Why the distinction matters

Telling an athlete’s heart apart from heart muscle disease is not an academic exercise. In a US registry of 1866 young competitive athletes who died suddenly or survived cardiac arrest between 1980 and 2006, 1049 events (56%) had a cardiovascular cause.[10] The most common cardiovascular causes reported were hypertrophic cardiomyopathy (36%) and congenital coronary artery anomalies (17%).[10] These figures describe a registry covering 1980–2006 and should not be read as universal estimates for today’s athletes. The authors also stressed that the absolute number of cardiovascular sudden deaths in this registry was relatively low, under 100 per year.[10]

The athlete’s ECG

High QRS voltages are common in trained athletes. According to international consensus criteria, up to 64% of athletes meet the Sokolow-Lyon voltage criterion for left ventricular hypertrophy, and isolated voltage criteria are classified as a normal training-related finding that does not by itself require further evaluation in asymptomatic athletes without a significant family history or other concerning findings.[14] Isolated QRS voltage criteria for left ventricular hypertrophy, without other ECG abnormalities, are seen in fewer than 2% of patients with hypertrophic cardiomyopathy.[14] By contrast, high voltage combined with T-wave inversion, ST-segment depression or pathological Q waves should raise the possibility of pathological hypertrophy and prompt further evaluation.[14]

What happens when training stops

A reduction in wall thickness with detraining may help to distinguish physiological from pathological hypertrophy.[12] Six Olympic rowers and canoeists with septal thickening of 13–15 mm substantially reduced their training for 6–34 weeks (mean 13) after the 1988 Games.[12] Mean maximum septal thickness fell from 13.8 mm to 10.5 mm, a change the authors considered strongly suggestive of training-induced, physiological hypertrophy.[12]

The longer-term picture is more nuanced. In 40 elite male athletes with a cavity of 60 mm or more, a wall of 13 mm or more, or both, a mean of 5.6 years of detraining reduced cavity size by 7% (from 61.2 to 57.2 mm), maximum wall thickness by 15% (from 12.0 to 10.1 mm) and height-indexed left ventricular mass by 28%.[9] Wall thickness returned to normal in every athlete, but 9 athletes (22%) still had a cavity of 60 mm or more; about half of the incomplete reduction was explained by weight gain and continued recreational exercise.[9] None developed cardiac symptoms or left ventricular dysfunction, although the authors could not exclude long-term implications in some individuals.[9]

Anabolic Steroids and Heart Function

Heart findings in strength athletes are not always explained by training alone. In a cross-sectional study of experienced male weightlifters aged 34–54, 86 men with at least two years of cumulative anabolic-androgenic steroid use were compared with 54 weightlifters who had never used them.[15] Steroid users had a lower left ventricular ejection fraction (52% versus 63%), and men who were using steroids at the time of testing had a lower ejection fraction (49%) than those who were currently off steroids (58%).[15] The design was observational, so it shows an association rather than proof of cause, but it is a reminder that a strength athlete’s heart findings may need to be interpreted with the full history in mind.

When the Finding Needs a Closer Look

Taken together, the studies above describe several situations in which the finding is less likely to be a benign variant:

Reduced systolic function or regional wall-motion abnormalities, which were not part of the physiological pattern described in elite athletes with cavity enlargement.[7]
Increased left ventricular wall thickness that is not explained by loading conditions such as training or high blood pressure; in elite athletes, a wall of 13 mm or more was rare and occurred together with an enlarged cavity.[8][13]
ECG voltage criteria accompanied by T-wave inversion, ST-segment depression or pathological Q waves.[14]
Hypertrophy in the setting of high blood pressure or obesity, where left ventricular mass is linked to cardiovascular risk.[2][3][4]

In practice, such findings are interpreted together with symptoms, history and imaging, often in consultation with a cardiologist.

Conclusion: Enlarged Heart

An enlarged heart is a description that needs context. In the studies reviewed here, high blood pressure and obesity were both closely linked to left ventricular hypertrophy, which was found in 36–41% of hypertensive patients and 56.0% of obese individuals.[3][4] Higher left ventricular mass predicted cardiovascular events and death in people without clinically apparent cardiovascular disease, and regression of hypertrophy or persistently normal mass was associated with fewer events than persistent or new hypertrophy.[2][6] A chest X-ray may miss cardiomegaly, ECG voltage criteria have low sensitivity for left ventricular hypertrophy in hypertension, and echocardiography served as the reference standard for heart size in the X-ray study.[1][5]

In elite athletes, a large left ventricle with normal function was often interpreted as physiological: 14% of elite athletes had a cavity of 60 mm or more, while a wall of 13 mm or more was rare (1.7% of 947 elite athletes).[7][8] Separating this from hypertrophic cardiomyopathy matters, because it was the most common cardiovascular cause of sudden death reported in a large registry of young US athletes covering 1980–2006.[10]

This matches what I see in practice. In my patients, an enlarged heart most often reflects left ventricular hypertrophy from long-standing high blood pressure, and in my view the most important step is first to find and recognise these patients, and then to treat the risk factors and the underlying cause. For most of my patients, the main risk factor is high blood pressure, which warrants treatment. From a clinical perspective, other investigations are then carried out for differential diagnosis, sometimes in collaboration with a cardiologist, particularly if there are any signs of heart failure. An athlete’s slow heart rate and normal or low blood pressure contrast with the clearly raised office readings I tend to see in hypertensive hypertrophy, and patients with a family history of inherited cardiomyopathy may need a referral for further investigation. Heart rate and blood pressure are contextual clues only and are not sufficient on their own to separate an athlete’s heart from heart disease.

Enlarged Heart: Causes, Diagnosis, Risk — and When an Athlete’s Heart Is Normal

Table of Contents

Key Takeaways: Enlarged Heart

Introduction: Enlarged Heart

What Does “Enlarged Heart” Actually Mean?