Delayed Treatment of Acute Myocardial Infarction With Ventricular Septal Rupture Due to Patient Fear During the COVID-19 Pandemic.

During the coronavirus disease 2019 (COVID-19) pandmic, more patients are presenting with complications late after acute myocardial infarction. We report the case of a 71-year-old man who delayed seeking medical care for 2 weeks, despite progressive shortness of breath, cough, and tactile fever, for fear of contracting COVID-19 in the hospital. Clinical and echocardiographic evaluation revealed a ventricular septal rupture secondary to acute myocardial infarction. The patient underwent urgent cardiac catheterization, followed by successful saphenous vein grafting to the left anterior descending coronary artery and open surgical repair of the ventricular septal rupture with a bovine pericardial patch. This case highlights a potential long-lasting negative effect that the COVID-19 pandemic will have on the care-seeking behavior and health of patients with acute cardiovascular disease.

Impact of hospital transfer to hubs on outcomes of cardiogenic shock in the real world.

AIMS: Cardiogenic shock (CS) is associated with significant mortality, and there is a movement towards regional 'hub-and-spoke' triage systems to coordinate care and resources. Limited data exist on outcomes of patients treated at CS transfer hubs. METHODS AND RESULTS: Cardiogenic shock hospitalizations were obtained from the Nationwide Readmissions Database 2010-2014. Centres receiving any interhospital transfers with CS in a given year were classified as CS transfer 'hubs'; those without transfers were classified as 'spokes.' In-hospital mortality was compared among three cohorts: (A) direct admissions to spokes, (B) direct admissions to hubs, and (C) interhospital transfer to hubs. Among hospitals treating CS, 70.6% were classified as spokes and 29.4% as hubs. A total of 130 656 (31.7%) hospitalizations with CS were direct admission to spokes, 253 234 (61.4%) were direct admissions to hubs, and 28 777 (7.0%) were transfer to hubs. CS mortality was 47.8% at spoke hospitals and was lower at hub hospitals, both for directly admitted (39.3%, P < 0.01) and transferred (33.4%, P < 0.01) patients. Hospitalizations at hubs had higher procedural frequency (including coronary artery bypass graft, right heart catheterization, mechanical circulatory support), greater length of stay, and greater costs. On multivariable analysis, direct admission to CS hubs [odds ratio (OR) 0.86, 95% confidence interval (CI) 0.84-0.89, P < 0.01] and transfer to hubs (OR 0.72, 95% CI 0.69-0.76, P < 0.01) were both associated with lower mortality. CONCLUSION: While acknowledging the limited ability of the Nationwide Readmissions Database to classify CS severity on presentation, treatment of CS at transfer hubs was associated with significantly lower mortality within this large real-world sample.

Pseudo-Wellens syndrome from sepsis-induced cardiomyopathy: a case report and review of the literature.

BACKGROUND: Pseudo-Wellens syndrome is a rare entity characterized by the presence of electrocardiogram (ECG) changes of Wellens syndrome but without the stenosis of the left anterior descending (LAD) coronary artery. In previous reports, pseudo-Wellens syndrome most commonly resulted from recreational drug use or unidentified etiologies. We present a unique case of pseudo-Wellens syndrome due to sepsis-induced cardiomyopathy and a review of the literature. CASE PRESENTATION: A 62-year-old Caucasian woman was admitted for sepsis from left foot cellulitis. Laboratory data were notable for elevated lactate of 2.5 mmol/L and evidence of acute kidney injury. She developed chest pain on the third day of hospitalization. ECG showed symmetric T-wave inversion in leads V1-V4. Serial troponin I levels were within normal limits. Chest imaging showed no pulmonary embolism. Echocardiogram showed ejection fraction of 25%, left ventricular diastolic diameter of 4.6 cm, and multiple segmental wall motion abnormalities. Cardiac catheterization showed patent coronary arteries. The hospital course was complicated by transient sinus bradycardia and hypotension. She was hospitalized for a total of 17 days. ECG prior to discharge showed resolution of T-wave changes. CONCLUSION: Pseudo-Wellens syndrome may result from myocardial ischemia due to vasospasm or myocardial edema from external insults. In our case, we suspect sepsis-related cytokine production resulting in cardiomyopathy and pseudo-Wellens syndrome. The clinical manifestations were indistinguishable between Wellens and pseudo-Wellens syndrome. Physicians should include the diagnosis of pseudo-Wellens syndrome when considering the presence of LAD coronary artery occlusion given risk stratifications.

Elevated Cardiac Troponin in Acute Stroke without Acute Coronary Syndrome Predicts Long-Term Adverse Cardiovascular Outcomes.

Background. Elevated cardiac troponin in acute stroke in absence of acute coronary syndrome (ACS) has unclear long-term outcomes. Methods. Retrospective analysis of 566 patients admitted to Temple University Hospital from 2008 to 2010 for acute stroke was performed. Patients were included if cardiac troponin I was measured and had no evidence of ACS and an echocardiogram was performed. Of 200 patients who met the criteria, baseline characteristics, electrocardiograms, and major adverse cardiovascular events (MACE) were reviewed. Patients were characterized into two groups with normal and elevated troponins. Primary end point was nonfatal myocardial infarction during follow-up period after discharge. The secondary end points were MACE and death from any cause. Results. For 200 patients, 17 patients had positive troponins. Baseline characteristics were as follows: age 63.1 ± 13.8, 64% African Americans, 78% with hypertension, and 22% with previous CVA. During mean follow-up of 20.1 months, 7 patients (41.2%) in elevated troponin and 6 (3.3%) patients in normal troponin group had nonfatal myocardial infarction (P = 0.0001). MACE (41.2% versus 14.2%, P = 0.01) and death from any cause (41.2% versus 14.5%, P = 0.017) were significant in the positive troponin group. Conclusions. Elevated cardiac troponin in patients with acute stroke and no evidence of ACS is strong predictor of long-term cardiac outcomes.