Amir Darki

Spontaneous coronary artery dissection (SCAD) and stress-induced cardiomyopathy (SIC), or Takotsubo syndrome, are distinct nonatherosclerotic causes of acute coronary syndrome that predominantly affect women and share physical and emotional triggers. Their simultaneous occurrence is uncommon and presents diagnostic and therapeutic challenges. We report a 74-year-old woman with hypertension and a prior cerebrovascular accident who presented with severe, persistent chest pain and a high-sensitivity troponin level of 9,143 ng/L. She was diagnosed with non-ST-segment elevation myocardial infarction and treated with intravenous heparin and nitroglycerin. Because of persistent symptoms and high-risk features, urgent coronary angiography was performed and demonstrated SCAD involving the apical left anterior descending coronary artery. Echocardiogram demonstrated apical ballooning with preserved basal contractility, raising concern for concomitant SIC. Myocardial infarction due to SCAD remained in the differential diagnosis. The patient was initially hemodynamically stable following catheterization with plans to obtain a cardiac MRI for further evaluation; however, on hospital day 2, she developed complete heart block that progressed to asystolic cardiac arrest, and she died despite prolonged resuscitative efforts. This case highlights the potential coexistence of SCAD and SIC, and emphasizes the importance of carefully evaluating patients with apparent Takotsubo cardiomyopathy for concomitant coronary pathology. It also illustrates the potential electrical and clinical complications associated with these overlapping conditions and supports a possible shared catecholamine-mediated or bidirectional pathophysiologic relationship.

Background: Immune checkpoint inhibitors (ICIs) are effective antineoplastic agents but can cause adverse effects in many organ systems. Cardiovascular toxicities include arrhythmias, myocarditis, heart failure, takotsubo syndrome, pericarditis, coronary artery disease, and vasculitis. Case summary: A 66-year-old woman with Stage 3C2 endometrial carcinoma presented for her second cycle of pembrolizumab, carboplatin, and paclitaxel. She subsequently suffered cardiac arrest and was brought to the emergency department. Spontaneous circulation returned following resuscitation, but she was haemodynamically unstable. An electrocardiogram revealed complete heart block. Initial management included intubation, vasopressor support, and transcutaneous pacing before transfer to the catheterization lab. Coronary angiography revealed no coronary artery disease. Right heart catheterization confirmed severe cardiogenic shock despite inotropic support and a temporary transvenous pacemaker in place. A micro-axial flow pump (Impella CP) was implanted for deteriorating cardiogenic shock. She was treated with high-dose corticosteroids (dexamethasone 190 mg i.v.) for suspected ICI-associated myocarditis, with significant improvement in cardiac function. The Impella was weaned and removed on Day 5. Cardiac magnetic resonance imaging showed elevated T1 and T2 signal intensities, consistent with the 2018 Lake Louise Criteria for myocarditis. The complete heart block was resolved, but a leadless pacemaker was implanted due to pre-existing conduction abnormalities. Discussion: Early recognition of ICI-associated myocarditis can be achieved with biochemical testing, electrocardiography, imaging, and expedited investigation of alternative causes for cardiac decompensation. Our case demonstrates that temporary left ventricular assist devices can support cardiac output for patients in cardiogenic shock due to ICI-associated myocarditis, allowing for recovery following high-dose corticosteroids.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a complication of incomplete resolution of acute pulmonary embolism. We hypothesize changes in CT Hounsfield Unit gradient (HU-Δ) created by the dispersion of IV contrast through the downstream blood pool correlate with cardiac index (CI). We sought to compare HU-Δ with invasively obtained CI. Methods: We completed a retrospective analysis of CTEPH patients in which individuals with low CI (2) were identified. Both absolute and fractional HU-Δ were derived from pulmonary CTA by subtracting the HU value of the left atrium (LA) and left ventricle (LV) from the main pulmonary artery (MPA) (absolute) and expressing them as a percentage of MPA-HU (fractional) on static axial images. These were compared between low and normal CI. Results: Of the 237 patients, 50.2% were female, 53.2% were White, 36.7% were Black. Hemodynamics were mean pulmonary artery (PA) pressure = 45.4 ± 11.2-mmHg, pulmonary vascular resistance = 9.2 ± 4.4-WU, CI = 2.05 ± 0.48-L/min/m². There was a higher mean MPA-HU = 391.1 ± 113.6 than LA-HU = 251.6 ± 81. In patients with low CI, the HU-Δ was higher, HU-ΔMPA-LA was 148.9 ± 78.4 vs. 124.5 ± 77.2 (p = 0.02), and HU-ΔMPA-LV was 170.7 ± 87 vs. 140 ± 82 (p = 0.009). A HU-ΔMPA-LA = 118 had a sensitivity of 75.6% and specificity of 77% to detect low CI, AUC 0.61, p = 0.003. A HU-ΔPA-LV = 156 had a sensitivity of 77% and specificity of 53% to detect low CI, AUC = 0.62, p = 0.001. A fractional reduction HU-ΔMPA-LA of 35% had a sensitivity and specificity of 79% and 53%, respectively, to detect low CI (AUC 0.65, p < 0.001). A fractional reduction of the HU-ΔMPA-LV of 40% had a sensitivity and specificity of 80% and 55%, respectively, to detect low CI (AUC 0.65, p < 0.001). HU Δ were highly reproducible (Kappa = 0.9, p < 0.001, 95% CI 0.86–0.95). Conclusions: High HU Δ between MPA-LA and MPA-LV were associated with low CI in patients with CTEPH.

Partial anomalous pulmonary venous connection (PAPVC) is a rare congenital heart disease in which one or more pulmonary veins drain into the systemic venous circulation. The abnormal connection between the pulmonary vein and the right atrium can result in a right-sided volume overload due to a left-to-right shunt, followed by eventual right-sided pressure overload and right ventricular failure. PAPVC is usually associated with an atrial septal defect but can present as an isolated finding. We present a case of isolated PAPVC resulting in right heart failure and predominantly pre-capillary pulmonary hypertension. We discuss the challenges in the diagnosis and medical management of isolated PAPVC and highlight the clinical and hemodynamic indications for pulmonary vasodilators and diuretics.