Spontaneous Coronary Artery Dissection in Patients with Autosomal Dominant Polycystic Kidney Disease: A Systematic Review of the Literature

Author:

Milutinovic Stefan1ORCID,Bell Abraham1,Jancic Predrag2ORCID,Stanojevic Dragana3ORCID,Borghol Abdul Hamid4,Mina Jonathan5,Chebib Fouad T.4,Khambati Ibrahim6,Escarcega Ricardo O.17,Wood Malissa J.7

Affiliation:

1. Internal Medicine Residency Program at Lee Health, Florida State University College of Medicine, Cape Coral, FL 33909, USA

2. Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia

3. Clinic for Cardiology, University Clinical Center Nis, 18000 Nis, Serbia

4. Division of Nephrology and Hypertension, Mayo Clinic, Jacksonville, FL 32224, USA

5. Department of Internal Medicine, Staten Island University Hospital, Northwell Health, Staten Island, NY 10305, USA

6. Associates in Nephrology, Cape Coral, FL 33909, USA

7. Lee Health Heart Institute, Fort Myers, FL 33908, USA

Abstract

Spontaneous coronary artery dissection (SCAD) is a spontaneous intimal tear of the coronary artery wall. A factor rarely associated with SCAD is autosomal dominant polycystic kidney disease (ADPKD). Using the PRISMA guidelines, we identified 10 unique cases of SCAD in ADPKD patients reported between 1998 and 2021. Ages ranged from 36 to 59 years, with an average of 44.6 years. The majority of patients were female (80%). Each case was diagnosed with a cardiovascular event: ST-elevation myocardial infarction (STEMI) in 40%, non-ST elevation myocardial infarction (NSTEMI) in 50%, and stable angina in 10%. Conservative management was used in 60% of cases. There is a significant gap in our understanding of the relationship between SCAD and ADPKD. Polycystin complex can lead to structural abnormalities in blood vessels, resulting in vascular leaks and vessel rupture. This suggests that ADPKD patients may have an elevated risk of arteriopathies, including coronary artery dissection.

Publisher

MDPI AG

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