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Cardiovascular complications are a frequent occurrence in SARS-CoV-2 infection. Takotsubo cardiomyopathy (also known as stress cardiomyopathy) is a possible cause of transient ST segment elevation (1–3% of total cases) and is characterized by a reversible left ventricular dysfunction with coronary arteries free from critical stenosis. The predominant echocardiographic pattern of this cardiomyopathy is an akinesia of the mid-apical myocardial segments (‘apical ballooning’), with preserved kinetics of the basal segments. The incidence of Takotsubo cardiomyopathy showed a marked increase during the COVID-19 pandemic. The data showed that three factors mainly contribute to the onset of cardiomyopathy in patients with COVID-19: cytokine storm, adrenergic hyperactivation and microvascular dysfunction. A 79-year-old woman was hospitalized in the Pneumology department of our hospital for acute hypoxemic respiratory failure due to bilateral interstitial pneumonia SARS-CoV-2 related. In remote medical history: in 2010 diagnosis of breast cancer, treated with quadrantectomy, adjuvant chemo- and radiotherapy, with negative follow-up for disease recovery, systemic arterial hypertension, hypercholesterolaemia and from 2016 syndrome of reduced mobility as a result of a previous ischaemic stroke. Non-invasive mechanical ventilation with c-PAP was started in the ward and, for the detection of anterolateral electrocardiographic anomalies (diffuse symmetrical negative T waves. Figure) and an increase in myocardionecrosis markers (troponin I peak: 5.4 ng/ml), in the absence of chest pain or equivalent, echocardiographic evaluation was performed, which revealed an akinesia of the mid-apical segments of the left ventricle with preserved kinetics of the basal segments and severely depressed global systolic function (ejection fraction: 30%). BNP (18.100 pg/ml), interleukin-6 (339 pg/ml), and CRP (136 mg/l) were elevated on blood chemistry tests. In the suspicion of Takotsubo cardiomyopathy (InterTAK Score: 67, probability: 79.8%), cardioprotective therapy with ACE inhibitor, beta-blocker, diuretics, low molecular weight heparin, double antiaggregation, and statin was started, deferring coronary angiography to improve clinical conditions. In the following days, due to the respiratory and haemodynamic worsening, the patient was transferred to an intensive setting, where she was intubated and treated with levosimendan and noradrenaline. In the intensive care unit, serial echocardiograms (over 30 days) showed a progressive improvement, up to normalization, of the global systolic function (ejection fraction at the last checkup: 55%), with complete regression of the kinetic anomalies, confirming the diagnostic hypothesis of stress cardiomyopathy. For a pulmonary mycotic superinfection (positive bronchoaspirate for Candida albicans and Candida krusei), complicated by iatrogenic pneumothorax, in the following days the patient died.

Already from the first data in China in early 2020 it emerged that patients with cardiovascular comorbidities had an increased risk of contracting SARS-CoV-2 infection and a more unfavourable clinical course. From March to May 2020, 85 patients affected by COVID-19 were enrolled, hospitalized at the Great Metropolitan Hospital of Reggio Calabria. The mean age was 63.6 ± 16.5 years. All patients underwent anamnesis, clinical evaluation, chest CT, ECG and measurement of markers of cardiovascular damage (Troponin I, CK-MB, LDH, D-dimer, BNP) and of inflammation (PCR, IL-6, and PCT). Thirty-one patients underwent echocardiography to look for signs of left ventricular dysfunction and/or repercussions of lung disease on the right sections. In particular, we evaluated parietal dimensions and thicknesses, biventricular function and transvalvular tricuspid and pulmonary flows and correlated the data obtained with ECG, radiological, clinical, and biohumoral parameters. The aim of our study was to evaluate the prognostic impact of cardiovascular involvement in COVID-19, investigating the effect of cardiovascular risk factors, levels of cardiovascular damage markers and newly emerging ECG and echocardiographic changes on a composite primary endpoint, consisting of the combination of exitus and the need for intensive care (ICU). For this purpose, the enrolled patients were divided into two subpopulations: those with better prognosis and those with poorer prognosis (ICU/exitus). We then analysed the reciprocal correlation of each of the investigated parameters and searched for the presence of echocardiographic signs of repercussion on the right sections of the pulmonary pathology. Among the patients with the poorest prognosis, 81.2% were hypertensive, 12.5% diabetic, 25% dyslipidaemic. Comparing the two subpopulations analysed, it emerged that patients with the worst prognosis were known hypertensive (P 0.02). Longer QTc intervals were associated with higher levels of CRP (P

Hypertrophic cardiomyopathy (HCM) is the most frequent genetic disease of the myocardium, with a prevalence of 1:500 cases in the general population. The salient feature is a hypertrophy, symmetrical or not, of the walls of the left ventricle (mainly the septum, but also less typical locations, such as the apex or the infero-lateral wall), not linked to abnormal load conditions. HCM is mostly an autosomal dominant inherited disease with incomplete penetrance and variable expressivity, mainly linked to mutations in genes coding for sarcomeric proteins. Several studies have shown an up-regulation of the ACE-2 gene, perhaps indicative of a compensatory anti-hypertrophic and anti-fibrotic response of the myocardium, in hypertrophic cardiomyopathy. Being the ACE-2 receptor target of the Sars-CoV-2 virus, these patients may have an increased risk of infection and a worse outcome. A 47-year-old man, with no known comorbidities, was hospitalized in our Emergency Medicine Department for bilateral Sars-CoV-2 pneumonia. Noninvasive mechanical ventilation c-PAP (FiO2 60%, PEEP 7.5 cmH20) was started for hypoxemic respiratory failure and an ECG showed diffuse ventricular repolarization abnormalities suggestive of left overload (asymmetric negative T waves V4 to V6, in I, II and aVL, flat in aVF. Figure 1), with a deep Q wave in III. The patient was asymptomatic for chest pain and equivalents and D-dimer and indices of myocardionecrosis were normal. Echocardiographic evaluation was performed, with evidence of marked asymmetric concentric hypertrophy of the left ventricle (interventricular septum: 16 mm), without significant anomalies in segmental kinetics, noteworthy valvulopathies and pericardial effusion. The family and personal medical history were negative for syncope, sudden cardiac death and resuscitated cardiac arrest and the estimated risk of sudden cardiac death at five years (HCM Risk-SCD) was