Background: We present a case of a young female with no pre-existent conditions, who presented to the hospital one month after a mild COVID-19 infection with severe myocarditis complicated by cardiogenic shock. Case: A 40-year-old female with no prior medical history and a regular, vigorous exercise program developed a mild COVID-19 infection with symptoms of mild fatigue, myalgias, chills, fever, and loss of taste, which resolved within a week. A month later, she presented to the hospital with exertional dyspnea, weakness, chest pressure, abdominal pain, and fatigue. A transthoracic echocardiogram revealed a left ventricular ejection fraction of 15% with a severely dilated left ventricle, global hypokinesis and severe mitral regurgitation. Right heart catheterization demonstrated cardiogenic shock with a cardiac index of 1.4 liters per minute by Fick equation, and she was admitted to the cardiac intensive care unit. Cardiac magnetic resonance revealed subepicardial delayed enhancement along the lateral and inferolateral walls and elevated T1 mapping consistent with myocarditis. A right ventricle biopsy revealed myocyte hypertrophy and patchy interstitial fibrosis without evidence of inflammatory tissue. She was diuresed, supported with inotropic therapy, and empirically treated with high doses of glucocorticoids. She clinically improved with weaning of inotropes and was discharged in stable condition on goal-directed medical therapy after 2.5 weeks. Conclusion: This patient represents a case of severe cardiogenic shock, after initial infection and in the absence of previously identified risk factors for development of COVID myocarditis. The absence of inflammatory tissue on pathology raises questions regarding the centrality of inflammatory processes in COVID-19-related myocardial injury leading to “long COVID” syndrome. These findings indicate the need for ongoing investigation of the long-term cardiovascular consequences of COVID-19.
Introduction: Takotsubo Syndrome (TTS), also known as Stress Induced Cardiomyopathy, is characterized by reversible left ventricular dysfunction without obstructive coronary disease, and largely affects post-menopausal women. However, limited data suggest increased mortality risk in men. We sought to compare national in-hospital outcomes between men and women admitted with TTS. Methods: All patients above 18 years who were admitted with primary diagnosis of TTS between 2012-2017 were identified by International Classification of Diseases (ICD)-9 and ICD-10 diagnostic codes in the National Inpatient Sample (NIS) Database. The primary endpoint was in-hospital all-cause mortality. Secondary endpoints included in-hospital complications, total cost, and duration of hospitalization. Results: A total of 8732 patients (90.8% female) were admitted with primary diagnosis of TTS. Women with TTS were older compared to men (66.9±12.4 vs. 63.1±15.7 years, p<0.001). However, men had increased tobacco use (48.8% vs 37.2%), alcohol use (11.6% vs 3.1%), and coronary artery disease (47.0% vs 39.7%, p<0.001 for all). Prevalence of diabetes, hypertension, atrial fibrillation, anemia, and heart failure was similar between groups. Men more frequently developed cardiogenic shock (7.1% vs 4.4%, p<0.001) requiring mechanical circulatory support (2.9% vs 1.7%, p=0.01), and had greater all-cause mortality compared to women (2.5% vs 1.4%, p=0.01). Using a multivariate regression model to adjust for age, race, substance use, and comorbidities, male gender (OR 2.12, 95% CI [1.69-2.68], p<0.001) and cardiogenic shock (OR 15.1, 95% CI [12.6-18.0], p<0.001) were associated with increased all-cause mortality. Lastly, men experienced greater length and cost of stay (4.0±4.2 vs. 3.6±3.6 days, and $56,428 vs. $46,908), fewer routine discharges (74.3% vs. 77.6%), and greater need for skilled nursing facility (11.6% vs. 9.2%, p<0.001 for all). Conclusion: TTS occurs predominantly in women but carries increased risk of in-hospital mortality in men, especially when complicated by cardiogenic shock. Perhaps improved risk stratification and early identification of patients with signs of shock or hemodynamic instability may help to improve outcomes.
To the Editor In their report of an inferior and anterior myocardial infarction (MI) owing to an occluded wraparound left anterior descending coronary artery (LAD), Kapil and colleagues 1 attribute the ST depression seen in lead V 2 to a reciprocal change owing to inferior wall involvement by the wraparound vessel. However, whereas leads I and especially aVL will typically manifest reciprocal ST depressions in inferior wall STEMI, this is not the case with lead V 2 unless there is involvement of the posterior wall. Furthermore, the structure of the ST segment in V 2 is not consistent with reciprocal change in this case where there is a broad-based upright T wave that the authors labeled as hyperacute in its form. Thus, rather than reciprocal change, the ST depression in V 2 is more likely an example of an evolving de Winter pattern of hyperacute T waves in acute anterior MI secondary to proximal LAD occlusion. 2 This pattern is characterized by upsloping ST depression and tall symmetric T waves in the precordial leads and is increasingly recognized as a STEMI equivalent requiring urgent revascularization. It is likely that had serial electrocardiograms been performed prior to percutaneous coronary intervention, a full-blown anterior STEMI pattern would have become evident.The authors also note that the algorithm by Fiol and colleagues 3 resulted in misidentification of the right coronary artery as the culprit vessel. However, the algorithm is only intended to predict whether the right coronary artery or left circumflex coronary artery is the culprit vessel for inferoposterior MI. The algorithm would not be appropriate to use when there is substantial electrocardiogram evidence of anterior MI owing to a LAD occlusion.
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