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. 2009 Oct;9(5):503–504. doi: 10.7861/clinmedicine.9-5-503a

Severe hypercalcaemia mimicking acute myocardial infarction

Rodney H Falk 1,
PMCID: PMC4953471  PMID: 19891057

Editor – The case report by Wesson and colleagues (Clin Med April 2009 pp 186–7) purports to show an electrocardiographic pattern of a myocardial infarct produced by hypercalcaemia. The authors base this supposition on the absence of elevation in cardiac enzymes and the lack of ST elevation over the 36 hours before death. However they presented no previous electrocardiogram (ECG) for comparison nor an echocardiogram at the time of the abnormality, and they noted a history of coronary artery disease and left-sided heart failure.

I would suggest that, rather than postulate a pseudo-infarct due to elevated serum calcium, the correct diagnosis is unrelated to hypercalcaemia and simply represents the presence of a left ventricular aneurysm, with anterior wall Q waves and persistent ST elevation. This would fit with the history of left ventricular (LV) failure and angioplasty and would explain the negative enzymes. Although hypercalcaemia has, on rare occasions, been described as mimicking ST elevation due to its effect on the ST segment, there is no reason that it would cause the pathologic Q waves seen in leads V1 to V5. In contrast, pathologic Q waves with persistent ST elevation are typical of LV aneurysm.

The case was described as a ‘lesson of the month’. I believe that the lesson here is not the one that was presented but just the opposite. From the presented data one can conclude that common things occur most commonly, incomplete data (lack of prior ECG and no echocardiogram) may lead to incorrect diagnosis, and that even reputable journals allow information to be published that is inaccurate and misleading.

Clinical Medicine. 2009 Oct;9(5):504.

Severe hypercalcaemia mimicking acute myocardial infarction

Laura Wesson 1,, Venk Suresh 2,

Sado and Greaves have raised the possibility of left ventricular (LV) aneurysm, hypertrophic cardiomyopathy (HOCM) and pericarditis as a differential diagnosis. Falk suggests that LV aneurysm was the most likely diagnosis. We agree that the points raised are valid. The patient certainly had a significant history of ischaemic heart disease. Her past cardiac history included non-ST elevation myocardial infarctions (NSTEMIs) with left ventricular failure (LVF). Seven months before the published event, she was admitted with NSTEMI and LVF. The angiogram showed normal left main stem, significant stenosis of left anterior descending (LAD) artery, moderate stenosis of distal right coronary artery, and obtuse marginal. She subsequently had elective percutaneous coronary intervention (PCI) to her LAD, with three bare metal stents, as there would have been difficulties to insert drug-eluting stents due to calcification and tortuosity. She had a further admission with NSTEMI and LVF three months before the published event, due to instent restenosis, which was treated with balloon dilatation only.

On both occasions the LV systolic function was well preserved with mild hypokinesia of the anteroapical and inferoapical walls; no evidence of LV aneurysm on either occasion. An echocardiogram (ECHO) at the time of the first PCI did not show any evidence of LVH or HOCM. Therefore we felt LV aneurysm or cardiomyopathy were unlikely based on previous investigations. Moreover the patient did not have any significant cardiac event between the last PCI and the published event. We agree that a repeat ECHO during the published admission (unfortunately not undertaken) or post-mortem (declined by family) would have clinched or refuted the differential diagnosis of LV aneurysm.

Supporting our theory, the most recent ECG before this published admission showed Q waves in V3 and V4 with ST coving and T wave inversion. Therefore we felt that the profound ST segment elevation during published admission was secondary to severe hypercalcaemia.

The chest pain history was not suggestive of pericarditis. As saddle-shaped ST elevation is only seen in V5, the ST segment elevation in other leads does not suggest pericarditis. Moreover the PQ/PR segment appears normal. Therefore we felt pericarditis to be an unlikely diagnosis. To conclude we feel that the ECG changes are secondary to profound hypercalcaemia rather than LV aneurysm or hypertrophic cardiomyopathy.


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