[Case of peripartum cardiomyopathy misdiagnosed as pulmonary changes due to COVID-19].

A 37-year-old female patient was admitted 16 days after delivery in a hospital for infectious diseases with cough, shortness of breath, and infiltrative changes in the lungs that were interpreted as viral pneumonia. Considering the failure of therapy and the history, peripartum cardiomyopathy was suspected. Examination revealed a decrease in left ventricular ejection fraction to 30 %, ultrasonic signs of lung congestion and bilateral hydrothorax. The patient was diagnosed with peripartum cardiomyopathy accompanied by functional class 4 heart failure. A specific feature of this case was fast positive dynamics with complete regression of the clinical picture of congestion and improvement of the left ventricular myocardial function associated with the treatment.

Covid-19 Infection During Pregnancy With Acute Heart Failure, Venous Thrombosis And Pneumonia.

The COVID-19 infection has spread rampantly, attaining pandemic status within three months of its first appearance. It has been classically associated with respiratory signs and symptoms. However, unusual presentations have also been reported in multiple literatures. We are reporting a case of acute heart failure in a pregnant patient diagnosed with Covid-19 infection. Her hospital course has been complicated by pneumonia and venous thrombosis during the postpartum period. Her laboratory investigations showed evidence of myocardial injury, acute heart failure, and COVID-19 infection in second PCR sample taken during postpartum period. Echocardiography exhibited features of severe left ventricle systolic dysfunction. She had successful delivery through caesarean-section, nevertheless, her postpartum period was complicated by pneumonia and right femoral venous thrombosis. CT scan of the chest and pulmonary arteries revealed infiltrations in the left lower lobe and right middle lobe, suggestive of consolidation, with no evidence of pulmonary embolism. Cardiac MRI displayed severe global LV and RV systolic dysfunction, but no evidence of myocardial infarction, myocardial infiltration, or abnormal myocardial delayed enhancement. Her condition improved and she was discharged on heart failure medications. During follow-up at the heart failure clinic, her symptoms continued to ameliorate, except the LV and RV systolic dysfunction which persisted. Multiple unusual presentations of Covid-19 infection have been reported in various literatures and screening of the COVID-19 infection should be practiced on regular basis especially among high-risk patients. Prompt identification of COVID-19 infection will lead to proper isolation and mitigation of infection spread among hospitalized patients and health care workers. Covid-19 PCR should be repeated in cases having clinical indication and negative first sample. A proper history and cardiac MRI can differentiate between different aetiologies of heart failure during pregnancy and peripartum COVID-19 infection. Adequate anticoagulation should be considered in COVID-19 patients due to the high risk of thromboembolism. Among patients with COVID-19 infection, CT chest helps demonstrate the extent of pulmonary involvement.

Stress-Induced Cardiomyopathy-Considerations for Diagnosis and Management during the COVID-19 Pandemic.

The novel coronavirus disease 2019 (COVID-19) is associated with several cardiovascular manifestations including myocardial injury, myocarditis, arrhythmia, and pulmonary embolism. Rare cases of stress-induced cardiomyopathy, or takotsubo syndrome have also been reported during the acute infection, and secondary to stress following lockdown and self-isolation. Diagnosis in the setting of the acute infection is challenging since conventional imaging modalities such as transthoracic echocardiography and coronary angiography should be restricted to minimize physician-patient contact until the patients is tested negative for COVID-19. The use of point of care hand-held ultrasound is appropriate for this purpose. The overall course of the disease seems to be similar to takotsubo in the general population. Physicians should be familiar with the clinical presentation, possible complications, and management of takotsubo during COVID-19 outbreak. Here, we review the special considerations in the diagnosis and management of takotsubo syndrome during the current pandemic.

Sjögren-related cardiomyopathy presenting with cardiogenic shock.

Previous reports have described non-ischaemic cardiomyopathy related to a variety of autoimmune diseases. However, very few case reports describe Sjögren disease as a contributing factor to cardiomyopathy. We report the case of a 69-year-old woman with a history of Sjögren disease who presented with cardiogenic shock. Laboratory testing and cardiac MRI revealing apical septal late gadolinium enhancement were consistent with an autoimmune aetiology. After ruling out ischaemic, infectious and other possible causes, the patient's clinical presentation was thought to be related to underlying Sjögren disease. She was treated with intravenous steroids and evidence-based heart failure therapy, but she eventually died after having declined heart transplantation. Given the rarity of Sjögren disease, no diagnostic criteria or standard treatment has been established for cardiomyopathy related to this disease. Diagnosis should be considered in patients who show evidence of autoimmune processes after other possible causes are ruled out.

Relationship of magnesemia with myocardial damage and mortality in patients with COVID-19.

Magnesium (Mg) is the second most abundant intracellular cation and plays a significant role in immune system and cardiac protection. Mg deficiency contributes to chronic low-grade inflammation leading to cardiovascular diseases, and low Mg level exacerbates virus-induced inflammation. The aim of the study was to investigate whether serum magnesium level is associated with myocardial damage and prognosis of COVID-19. This was a single-center, observational retrospective study of patients with COVID-19. The study population was divided into two groups according to in-hospital mortality: a survivor group (SG) and a non-survivor group (NSG). Myocardial damage was defined as blood levels of cardiac troponin I (cTnI) above the 99th percentile upper reference limit. Magnesium, variables regarding inflammation, and myocardial damage were compared between the groups. A total of 629 patients with COVID-19 were included. Mortality rate was 11.85% (n = 82). There were 61 (74.4%) and 294 male patients (53.7%) in NSG and SG, respectively (p = 0.001). The median age of NSG was 64.5 years (min-max: 37-93) and the median age of SG was 56.0 years (min-max: 22-92) (p < 0.001). Median serum magnesium levels of NSG and SG were 1.94 mg/dL (min-max: 1.04-2.87) and 2.03 mg/dL (min-max: 1.18-2.88), respectively (p = 0.027). Median cTnI levels of NSG and SG were 25.20 pg/mL (min-max: 2.10-2240.80) and 4.50 pg/mL (min-max: 0.50-984.3), respectively (p < 0.001). The cTnI levels were lower in those patients whose serum Mg levels were higher than 1.94. Although serum magnesium level was not a predictor for in-hospital mortality, there was a significant negative correlation between magnesemia and myocardial damage.

Isolated Right Ventricular Noncompaction Cardiomyopathy Causing Pulmonary Embolism.

Ventricular noncompaction is a rare, heterogeneous cardiomyopathy characterized by marked trabeculations and deep intertrabecular spaces with clinical sequelae of heart failure, arrhythmias, and cardioembolic events. In this article, we describe a patient with isolated right ventricular noncompaction who presented with submassive pulmonary embolism, which was managed with long-term direct oral anticoagulation.

[Update 2021: COVID-19 from the perspective of cardiology]. / Update 2021: COVID-19 aus Sicht der Kardiologie.

More than one year ago COVID-19 emerged to a rapidly expanding global pandemic. Along with a growing number of individuals infected with SARS-CoV-2, we gained substantial knowledge on development, progression and treatment of the disease. In the light of increasing worldwide infection rates during the current "third wave", we will give a short update on COVID-19 from a cardiological point-of-view.

T2-mapping increase is the prevalent imaging biomarker of myocardial involvement in active COVID-19: a Cardiovascular Magnetic Resonance study.

BACKGROUND: Early detection of myocardial involvement can be relevant in coronavirus disease 2019 (COVID-19) patients to timely target symptomatic treatment and decrease the occurrence of the cardiac sequelae of the infection. The aim of the present study was to assess the clinical value of cardiovascular magnetic resonance (CMR) in characterizing myocardial damage in active COVID-19 patients, through the correlation between qualitative and quantitative imaging biomarkers with clinical and laboratory evidence of myocardial injury. METHODS: In this retrospective observational cohort study, we enrolled 27 patients with diagnosis of active COVID-19 and suspected cardiac involvement, referred to our institution for CMR between March 2020 and January 2021. Clinical and laboratory characteristics, including high sensitivity troponin T (hs-cTnT), and CMR imaging data were obtained. Relationships between CMR parameters, clinical and laboratory findings were explored. Comparisons were made with age-, sex- and risk factor-matched control group of 27 individuals, including healthy controls and patients without other signs or history of myocardial disease, who underwent CMR examination between January 2020 and January 2021. RESULTS: The median (IQR) time interval between COVID-19 diagnosis and CMR examination was 20 (13.5-31.5) days. Hs-cTnT values were collected within 24 h prior to CMR and resulted abnormally increased in 18 patients (66.6%). A total of 20 cases (74%) presented tissue signal abnormalities, including increased myocardial native T1 (n = 11), myocardial T2 (n = 14) and extracellular volume fraction (ECV) (n = 10), late gadolinium enhancement (LGE) (n = 12) or pericardial enhancement (n = 2). A CMR diagnosis of myocarditis was established in 9 (33.3%), pericarditis in 2 (7.4%) and myocardial infarction with non-obstructive coronary arteries in 3 (11.11%) patients. T2 mapping values showed a moderate positive linear correlation with Hs-cTnT (r = 0.58; p = 0.002). A high degree positive linear correlation between ECV and Hs-cTnT was also found (r 0.77; p < 0.001). CONCLUSIONS: CMR allows in vivo recognition and characterization of myocardial damage in a cohort of selected COVID-19 individuals by means of a multiparametric scanning protocol including conventional imaging and T1-T2 mapping sequences. Abnormal T2 mapping was the most commonly abnormality observed in our cohort and positively correlated with hs-cTnT values, reflecting the predominant edematous changes characterizing the active phase of disease.

COVID-19 Severity Potentially Modulated by Cardiovascular-Disease-Associated Immune Dysregulation.

Patients with underlying cardiovascular conditions are particularly vulnerable to severe COVID-19. In this project, we aimed to characterize similarities in dysregulated immune pathways between COVID-19 patients and patients with cardiomyopathy, venous thromboembolism (VTE), or coronary artery disease (CAD). We hypothesized that these similarly dysregulated pathways may be critical to how cardiovascular diseases (CVDs) exacerbate COVID-19. To evaluate immune dysregulation in different diseases, we used four separate datasets, including RNA-sequencing data from human left ventricular cardiac muscle samples of patients with dilated or ischemic cardiomyopathy and healthy controls; RNA-sequencing data of whole blood samples from patients with single or recurrent event VTE and healthy controls; RNA-sequencing data of human peripheral blood mononuclear cells (PBMCs) from patients with and without obstructive CAD; and RNA-sequencing data of platelets from COVID-19 subjects and healthy controls. We found similar immune dysregulation profiles between patients with CVDs and COVID-19 patients. Interestingly, cardiomyopathy patients display the most similar immune landscape to COVID-19 patients. Additionally, COVID-19 patients experience greater upregulation of cytokine- and inflammasome-related genes than patients with CVDs. In all, patients with CVDs have a significant overlap of cytokine- and inflammasome-related gene expression profiles with that of COVID-19 patients, possibly explaining their greater vulnerability to severe COVID-19.

Sports Activity and Arrhythmic Risk in Cardiomyopathies and Channelopathies: A Critical Review of European Guidelines on Sports Cardiology in Patients with Cardiovascular Diseases.

The prediction and prevention of sudden cardiac death is the philosopher's stone of clinical cardiac electrophysiology. Sports can act as triggers of fatal arrhythmias and therefore it is essential to promptly frame the athlete at risk and to carefully evaluate the suitability for both competitive and recreational sports activity. A history of syncope or palpitations, the presence of premature ventricular complexes or more complex arrhythmias, a reduced left ventricular systolic function, or the presence of known or familiar heart disease should prompt a thorough evaluation with second level examinations. In this regard, cardiac magnetic resonance and electrophysiological study play important roles in the diagnostic work-up. The role of genetics is increasing both in cardiomyopathies and in channelopathies, and a careful evaluation must be focused on genotype positive/phenotype negative subjects. In addition to being a trigger for fatal arrhythmias in certain cardiomyopathies, sports also play a role in the progression of the disease itself, especially in the case arrhythmogenic right ventricular cardiomyopathy. In this paper, we review the latest European guidelines on sport cardiology in patients with cardiovascular diseases, focusing on arrhythmic risk stratification and the management of cardiomyopathies and channelopathies.

When cardiomyopathy, cancer, and COVID-19 collide: A case report.

Malignancy has historically prohibited solid organ transplant; however, patients with effectively treated, favorable-risk cancers should not necessarily be eliminated as transplant candidates. These cases require careful review by a multidisciplinary team. Here, we report the case of a woman with end-stage heart failure undergoing heart transplant evaluation during the COVID pandemic who was found to have early-stage, hormone receptor-positive breast cancer. Given her favorable cancer-related prognosis, a multidisciplinary committee recommended lumpectomy, accelerated partial breast irradiation, and adjuvant aromatase inhibitor therapy for definitive treatment to allow for consideration of orthotopic heart transplant.

Myocardium injury biomarkers predict prognosis of critically ill coronavirus disease 2019 (COVID-19) patients.

BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic is a once-in-century crisis to public health. Although the pathogen for COVID-19, the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has been identified, the pandemic is still ongoing. The critically ill COVID-19 patients account for most disease-associated death; thus, there is an urgent need to identify prognostic factors that would help determine therapeutic approaches. METHODS: In this study, we retrospectively analyzed the clinical and laboratory findings in 100 critically ill COVID-19 patients in Hubei Women & Children Healthcare Hospital (Guanggu District), of whom 22 patients died in hospital, and 78 patients survived. RESULTS: We found that age, lymphocyte count, and total bilirubin concentration were an independent prognostic factor for critically ill COVID-19 patients. Of particular importance, we observed a significant elevation of myocardium injury biomarkers, including CK-MB, high-sensitivity cardiac troponini I (hs-cTnI), and Mb, in the non-survivor group. These myocardium injury biomarkers appeared to correlate with the time of survival, and two multivariate models have suggested hs-cTnI was a novel prognostic factor with a sensitivity of 75.0% and a specificity of 84.9%. CONCLUSIONS: Altogether, our study highlighted the prognostic significance of myocardium injury biomarkers in critically ill COVID-19 patients. Monitoring myocardium injury biomarkers would predict patient survival and guide therapeutic strategy.

Non-invasive Thoracic Impedance Changes in COVID-19 Pulmonary Infection.

Graphical abstract.

Mechanisms and treatments of myocardial injury in patients with corona virus disease 2019.

The infection epidemic event of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was formally declared a pandemic by World Health Organization on March 11th, 2020. Corona Virus Disease 2019 (COVID-19) is caused by SARS-CoV-2, a new type of coronavirus, which has high contagion and mainly causes respiratory symptoms. With the increase in confirmed cases, however, the infection symptoms turn to be diverse with secondary or first clinical symptoms relating to damage of the cardiovascular system and changes of myocardial enzyme spectrum, cardiac troponin I, electrocardiogram, cardiac function. The occurrence of extra-pulmonary manifestations, including immediately and long-term damage, means that the overall health burden caused by SARS-CoV-2 infection may be under-estimated because COVID-19 patients developed cardiovascular system injury are more likely to become serious. The factors such as directly pathogen-mediated damage to cardiomyocytes, down-regulated angiotensin-converting enzyme 2 (ACE2) expression, excessive inflammatory response, hypoxia and adverse drug reaction, are closely related to the occurrence and development of the course of COVID-19. In combination with recently published medical data of patients having SARS-CoV-2 infection and the latest studies, the manifestations of damage to cardiovascular system by COVID-19, possible pathogenic mechanisms and advances of the treatment are proposed in this article.

Transient Cardiomyopathy in a Patient With Coronavirus Disease-2019.

A 66-year-old male patient with coronavirus disease-19 (COVID-19) developed cardiogenic shock with echocardiographic evidence of decreased left ventricular ejection fraction and global hypokinesia concomitant with a robust systemic inflammatory response. Following the administration of convalescent plasma therapy and inotropic support, left ventricular function recovered fully in accordance with the decrease in the concentration of the inflammatory markers. Thus, we demonstrate the presence of transient reversible cardiomyopathy in a patient with severe COVID-19 and illustrate the association of acute cardiac dysfunction with profound systemic inflammation among COVID-19 patients.