Comment on "A Rare Case of Renal Infarct due to Noncompaction Cardiomyopathy: A Case Report and Literature Review".

Josef Finsterer,Sinda Zarrouk-Mahjoub

doi:10.1155/2016/3240695

Abstract

With interest we read the article by Wats et al. about a 53-year-old female with left ventricular hypertrabeculation/noncompaction (LVHT) in whom renal infarction was attributed to LVHT [1]. We have the following comments and concerns.

Highlights

We do not agree with the statement that left ventricular hypertrabeculation/noncompaction (LVHT) is a genetic disease, due to an arrest in the embryonic compaction process
How can the authors be sure that renal infarction originated from LVHT and not from another source [1]? Were atrial fibrillation, heart failure, venous thrombosis, and patent foramen ovale excluded as source of embolism? The patient had an ejection fraction of 25% and dilated cardiomyopathy, conditions which are prone to cardiac embolism
Why did the authors not consider heart failure as the source of embolism? Were aortic plaques, aortic aneurysm, or renal artery stenosis excluded as causes of renal embolism? A further argument against LVHT as the source of embolism is that some studies have shown that the risk of systemic cardioembolism is not increased in patients with LVHT compared to the general population [2]

Summary

Introduction

We do not agree with the statement that LVHT is a genetic disease, due to an arrest in the embryonic compaction process. How can the authors be sure that renal infarction originated from LVHT and not from another source [1]? Heart failure, venous thrombosis, and patent foramen ovale excluded as source of embolism?

Results

Conclusion