Ischemic Heart Disease and Acute Chest Pain - Cases
Sohaib Ahmad Basharat, MD
Fellow in training
Loma Linda University Medical Center, California, United States
Sohaib Ahmad Basharat, MD
Fellow in training
Loma Linda University Medical Center, California, United States
Joseph Chung, MD
Fellow in training
Loma Linda University Medical Center, California, United States
Anas Alani
Attending Physician
Loma Linda University Medical Center, United States
Dmitry Abramov, MD
Attending Physician
Loma Linda University Medical Center, United States
Pooja Swamy, MD
Cardiologist
Loma Linda University Medical Center, United States
Shannon Kirk, MD
Attending Physician
Loma Linda University Medical Center, United States
Ramesh Bansal
Attending Physician
Loma Linda University Medical Center, United States
Purvi Parwani, MD
Assistant Professor of Medicine
Loma Linda University Medical Center
Redlands, California, United States
A 70-year-old male with history of hypertension and diabetes mellitus presented to outside hospital with chest pain and dyspnea for two weeks. Patient was hemodynamically stable. On examination, he had audible S1 and S2 without any murmurs. Bilateral 1+ pedal edema was noted. Rest of the examination was benign. EKG showed sinus rhythm with no ischemic changes. Laboratory data showed an elevated troponin hs of 180 ng/L consistent with NSTEMI. A coronary angiogram showed triple vessel disease with 95% stenosis of proximal LAD, 90% stenosis of distal RCA, and CTO of the mid circumflex artery. A transthoracic echocardiogram showed EF 45-50%, hypokinesis of the inferior, inferolateral walls, and an echolucent pouch in the inferolateral wall concerning for pseudoaneurysm. Cardiac CT was done for further evaluation (Image 2). Patient was transferred to our hospital for potential need for cardiac surgery with CABG and pseudo-aneurysm repair.
Diagnostic Techniques and Their Most Important Findings:
Repeat echocardiogram at our center showed the outpouching in question in basal inferolateral wall (12mm wide at the mouth and 15mm deep, see Image 1), During systole, however, some collapse of the outpouching was noted raising concern for a diverticulum as opposed to a pseudoaneurysm. There was moderate hypokinesis of basal to mid inferior wall and mild hypokinesis of mid inferolateral wall. CMR was performed for further evaluation and showed a small outpouching in the basal inferolateral wall with normal contraction of the surrounding myocardium. There was hypokinesis of the mid inferolateral wall but no hypokinesis or LGE of basal inferolateral wall. There was LGE in the inferior wall confirming an inferior infarct. CMR again showed some collapse of the cavity with systole. These findings were consistent with a diverticulum, as opposed to a pseudoaneurysm (Image 3).
Learning Points from this Case:
Differentiating benign LV outpouchings (e.g., diverticulum or crypt) from pathological (e.g. aneurysm or pseudoaneurysm) can be challenging. Accurate diagnosis is critical for appropriate management. LV diverticula are congenital cardiac malformations that show full wall thickness, compression during systole, and no LGE on CMR. Aneurysms are usually seen in infarcted myocardium, are wide-mouthed, show full wall thickness, and will have LGE on CMR. Pseudoaneurysms are also sequelae of myocardial infarction, show only pericardial lining, are narrow-mouthed, and will show LGE in the surrounding myocardium on CMR. In our case, small cavity size, full wall thickness, and partial systolic collapse confirmed the diagnosis of LV diverticulum.
Late presentation of acute myocardial infarction with multivessel CAD and presence of pseudoaneurysm, as was initially suspected in our case, would necessitate surgical repair. Benign diverticulum, on the other hand, does not require surgical repair and as such CABG and PCI can both be viable options for revascularization. After Heart team discussion, the patient was deemed a suitable candidate for PCI.