Aims Our aim was to describe the electrocardiographic features of critical COVID-19 patients. Methods and results We carried out a multicentric, cross-sectional, retrospective analysis of 431 consecutive COVID-19 patients hospitalized between 10 March and 14 April 2020 who died or were treated with invasive mechanical ventilation. This project is registered on ClinicalTrials.gov (identifier: NCT04367129). Standard ECG was recorded at hospital admission. ECG was abnormal in 93% of the patients. Atrial fibrillation/flutter was detected in 22% of the patients. ECG signs suggesting acute right ventricular pressure overload (RVPO) were detected in 30% of the patients. In particular, 43 (10%) patients had the S1Q3T3 pattern, 38 (9%) had incomplete right bundle branch block (RBBB), and 49 (11%) had complete RBBB. ECG signs of acute RVPO were not statistically different between patients with (n = 104) or without (n=327) invasive mechanical ventilation during ECG recording (36% vs. 28%, P = 0.10). Non-specific repolarization abnormalities and low QRS voltage in peripheral leads were present in 176 (41%) and 23 (5%), respectively. In four patients showing ST-segment elevation, acute myocardial infarction was confirmed with coronary angiography. No ST-T abnormalities suggestive of acute myocarditis were detected. In the subgroup of 110 patients where high-sensitivity troponin I was available, ECG features were not statistically different when stratified for above or below the 5 times upper reference limit value. Conclusions The ECG is abnormal in almost all critically ill COVID-19 patients and shows a large spectrum of abnormalities, with signs of acute RVPO in 30% of the patients. Rapid and simple identification of these cases with ECG at hospital admission can facilitate classification of the patients and provide pathophysiological insights.

Uric acid is the final product of purine metabolism. Classically it is recognized as the cause of gouty arthritis and kidney stones. Western civilization has increased serum levels of uric acid which is no longer considered a benign plasma solute. It has been postulated and recently demonstrated that it can penetrate cell membrane and exerts damaging intracellular actions such as oxidation and inflammation. These observations have stimulated several epidemiological researches suggesting that hyperuricemia is linked or even provokes hypertension and coronary artery disease. In this review we summarize the current evidences regarding uric acid which contribute in the pathophysiology of coronary artery disease.

In the last few years, many studies focused their attention on the relationship between chronic obstructive pulmonary disease (COPD) and ischemic heart disease (IHD), showing that these diseases are mutually influenced. Many different biological processes such as hypoxia, systemic inflammation, endothelial dysfunction, heightened platelet reactivity, arterial stiffness and right ventricle modification interact in the development of the COPD-IHD comorbidity, which therefore deserves special attention in early diagnosis and treatment. Patients with COPD-IHD comorbidity have a worst outcome, when compared to patients with only COPD or only IHD. These patients showed a significant increase on risk of adverse events and of hospital readmissions for recurrent myocardial infarction, heart failure, coronary revascularization, and acute exacerbation of COPD. Taken together, these complications determine a significant increase in mortality. In most cases death occurs for cardiovascular cause, soon after an acute exacerbation of COPD or a cardiovascular adverse event. Recent data regarding incidence, mechanisms and prognosis of this comorbidity, along with the development of new drugs and interventional approaches may improve the management and long-term outcome of COPD-IHD patients. The aim of this review is to describe the current knowledge on COPD-IHD comorbidity. Particularly, we focused our attention on underlying pathological mechanisms and on all treatment and strategies that may improve and optimize the clinical management of COPD-IHD patients.

Multimodality cardiac imaging as a guide for CRT implantation is useful to increase response rate.

wrong, an error that was confirmed by a number of completely unsuccessful clinical trials that failed to show the benefits with a range of putative infarct-reducing agents. The main reason for this discrepancy lay in the time of administration of the compounds (i.e., before the onset of ischemia in the experimental setting, after the infarct in the clinical one).It then became apparent that early reperfusion was a prerequisite for the salvage of ischemic tissue. At the same time, it became also evident that reperfusion per se can be, paradoxically, dangerous, increasing rather than reducing the extension of the infarct.The second line of research related to cardiac surgery. Quickly, coronary artery bypass became a standard procedure for patients with angina and, with the time, this was extended, although with poor results, to evolving myocardial infarction (MI). No doubt that the surgeons had the monopoly of reperfusion and indeed they managed to develop techniques such as cardioplegia and hypothermia able to protect against the damage induced by reperfusion. Once again, the success of these techniques relies on their application before induction of ischemia.The third line of research is linked to pharmacologists who, in parallel with surgeons and pathologists, questioned that the thrombus was the result of an infarct. They proved that, actually, it is the cause of the infarct and started to look at measures to dissolve the infarct-initiating thrombi. Medicine has been undergoing constant changes, with cardiology being arguably the fastest changing field of all. The evolution -or should we say the revolution -of reducing the progression of coronary atherosclerosis with aspirin, angiotensin enzyme inhibitors and cholesterol-lowering drugs had a remarkable effect on the treatment of coronary artery disease. But perhaps one of the most important changes in cardiology is the ability to reperfuse the ischemic myocardium and consequently to reduce the deleterious effects of acute ischemia. Interestingly, during the second half of the century, 4 independent and different streams of research were initiated and would culminate in the ability to reperfuse the ischemic human heart.The first line of research related to pathophysiology. The 1960 s witnessed a remarkable increase in the systematic study of (1) the nature of atheroma and thrombosis and (2) the metabolic, contractive, ultrastructural and electrophysiological consequences of myocardial ischemia. Later, in part because of the relative ease of restoring coronary flow, investigators, including the authors of this review, turned their attention to the effects of reperfusion. 1-4 The idea of protecting the ischemic myocardium soon attracted a lot of enthusiasm and a cornucopia of compounds such as β-blockers, calcium antagonists, antiinflammatory drugs, and vasodilators were administered to animals with results that appeared dramatically successful. In the 1970 s and 1980 s, however, it became clear that this approach was Tissue salvage of severely ischemic myocardiu...