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Introduction and objectives Despite advances in treatment, patients with acute myocardial infarction (AMI) still exhibit unfavorable short- and long-term prognoses. In addition, there is scant evidence about the clinical outcomes of patients with AMI and coronavirus disease 2019 (COVID-19). The objective of this study was to describe the clinical presentation, complications, and risk factors for mortality in patients admitted for AMI during the COVID-19 pandemic. Methods This prospective, multicenter, cohort study included all consecutive patients with AMI who underwent coronary angiography in a 30-day period corresponding chronologically with the COVID-19 outbreak (March 15 to April 15, 2020). Clinical presentations and outcomes were compared between COVID-19 and non-COVID-19 patients. The effect of COVID-19 on mortality was assessed by propensity score matching and with a multivariate logistic regression model. Results In total, 187 patients were admitted for AMI, 111 with ST-segment elevation AMI and 76 with non-ST-segment elevation AMI. Of these, 32 (17%) were diagnosed with COVID-19. GRACE score, Killip-Kimball classification, and several inflammatory markers were significantly higher in COVID-19-positive patients. Total and cardiovascular mortality were also significantly higher in COVID-19-positive patients (25% vs 3.8% [P 140 (OR, 23.45; 95%CI, 2.52–62.51; P = .005) and COVID-19 (OR, 6.61; 95%CI, 1.82-24.43; P = .02) were independent predictors of in-hospital death. Conclusions During this pandemic, a high GRACE score and COVID-19 were independent risk factors associated with higher in-hospital mortality.

Introduction and objectives Ivabradine is an inhibitor of the If channel, the main determinant of the pacemaker function of the sinus node. The drug has been approved for the treatment of angina and heart failure. There is some evidence of its role as an inhibitor of atrial-ventricular node (AVN) conduction. The aim of the BRAKE-AF project is to assess ivabradine use for rate control in atrial fibrillation (AF). Methods A multicenter, randomized, parallel, open-label, noninferiority phase III clinical trial will be conducted to compare ivabradine vs digoxin in 232 patients with uncontrolled permanent AF despite beta-blockers or calcium channel blockers. The primary efficacy endpoint is the reduction in daytime heart rate measured by 24-hour Holter monitoring at 3 months. This clinical trial will be supported by an electrophysiological study of the effect of ivabradine on the action potential of the human AVN. To do this, an experimental model will be used with Chinese hamster ovarium cells transfected with the DNA encoding the expression of the t channels involved in this action potential and recording of the ionic currents with patch clamp techniques. Results New data will be obtained on the effect of ivabradine on the human AVN and its safety and efficacy in patients with permanent AF. Conclusions The results of the BRAKE-AF project might allow inclusion of ivabradine within the limited arsenal of drugs currently available for rate control in AF. Clinical trial registration: http://www.clinicaltrials.gov . Identifier: NCT03718273 .

Introduction. We use clinical, ECG, and biochemical data to stratify risk in patients with chest pain without ST segment elevation. However, the prognostic performance of these studies in relation to time from onset of symptoms is unknown. Patients and method. In a single-center, prospective study, 321 consecutive patients who had been admitted in the emergency room with a suspected acute coronary syndrome without ST segment elevation were included in the study. Blood samples were collected for CK, CK-MB mass, myoglobin, and cardiac troponin T analysis 6, 12 and 18 hours after the onset of pain and other clinical and ECG data were recorded. Univariate and multivariate analysis was used to identify independent prognostic predictors 6 and 12 hours after the onset of chest pain. Results. Five variables were independent predictors of the recurrence of ischemia. The model correctly classified 82% of the patients. Age, history of coronary artery disease, prolonged chest pain at rest in the preceding 15 days, pain, ST-segment changes with pain, and cardiac troponin T in excess of 0.1 ng/m 12 hours after the onset of chest pain were identified by logistic regression. A similar model was analyzed at 6 hours, after changing the cutoff point for cardiac troponin T. Cardiac troponin T was considered positive with values of 0.04 ng/ml 6 hours after the onset of chest pain. Conclusions. More than 80% of the patients admitted to the emergency room with chest pain without ST segment elevation can be correctly classified for new ischemic recurrences using clinical, ECG, and biochemical parameters 6 hours after the onset of pain.

Background. The prognostic value of biochemical markers in relation to time since onset of chest pain was evaluated in an emergency room with a chest pain unit. Methods. In a single-center, prospective study we included 321 consecutive patients admitted to the emergency room with suspected unstable angina IIIB and an evolution of less than 12 hours. Blood samples were collected for CPK, CPK MB mass, myoglobin, and cardiac troponin T assays 6, 12, and 18 h after the onset of pain. ROC curve analysis was carried out to compare biochemical markers in terms of cutoff values and time since onset of pain. We determined the relation between prognosis and biochemical markers before and after adjustment for baseline characteristics. Results. CPK mass and myoglobin showed the maximum sensitivity and specificity for new ischemic recurrences 6 hours after the onset of chest pain with laboratory cutoff values. We had to wait 12 h after the onset of pain for troponin T to be useful using the laboratory cutoff value (0.1 ng/ml). A single determination 6 hours after onset of chest pain of cardiac troponin T above 0.04 ng/ml was the most sensitive and specific marker for new ischemic recurrences. Conclusions. A single blood determination of cardiac troponin T 6 hours after the onset of chest pain complete the prognostic stratification in combination with clinical and ECG variables. The best cutoff point of cardiac troponin T, based on univariate and multivariate analysis, was 0.04 ng/ml 6 h after the onset of chest pain.

Coronary artery disease (CAD) and obstructive sleep apnea (OSA) are both complex and significant clinical problems. The pathophysiological mechanisms that link OSA with CAD are complex and can influence the broad spectrum of conditions caused by CAD, from subclinical atherosclerosis to myocardial infarction. OSA remains a significant clinical problem among patients with CAD, and evidence suggesting its role as a risk factor for CAD is growing. Furthermore, increasing data support that CAD prognosis may be influenced by OSA and its treatment by continuous positive airway pressure (CPAP) therapy. However, stronger evidence is needed to definitely answer these questions. This paper focuses on the relationship between OSA and CAD from the pathophysiological effects of OSA in CAD, to the clinical implications of OSA and its treatment in CAD patients.

There are limited data regarding the need for intensive care or the appropriate length of hospital stay for patients with ST elevation acute myocardial infarction (STEMI). In order to optimize resources, we tried to determine the need of coronary care unit (CCU) admission for patients with STEMI who remained in Killip class I after a successful primary percutaneous coronary intervention (PPCI).From August of 2006 till June of 2008, we analyzed data from all patients admitted in our CCU who met these criteria, a total of 278. We prospectively recorded all in-hospital adverse events and event-free survival at 30 and 90 days (all cause death, stroke, new acute coronary syndrome or re-hospitalization due to heart failure). Medical treatment was optimized according to the current guidelines.A coronary stent was implanted in 96% of the patients. None of the patients had any adverse event that could not be resolved in a step-down unit. Survival at 30 and at 90 days was 99.6% and 98.3% respectively. Event-free survival was 97.3% at 30 days and 94.3% at 90 days. The median length of stay was three days in the CCU and five days in the hospital.Patients with STEMI treated with PPCI who remained in Killip class I after the procedure and receive optimal pharmacological treatment have an excellent prognosis. All of them can probably be admitted safely to a step-down unit. Wide application of this management strategy may result in substantial cost savings.