Despite advances in diagnostic and therapeutic interventions, coronary heart disease remains as one of the leading causes of death in developed countries. ST-segment elevation myocardial infarction is associated with the highest mortality and is an indication for emergent reperfusion therapy. Current guidelines for emergent reperfusion not only include ST segment elevations but also consider evidence of a new onset Left Bundle Branch Block (LBBB). However, accumulating evidence indicates that RBBB is also associated with poor outcome in coronary artery disease. To-date, guidelines do not comment on the urgency of reperfusion therapy with sole evidence of a new onset Right Bundle Branch Block (RBBB). Particularly we question whether clinicians should focus on new-onset RBBB as a ST-segment elevation equivalent. If so, appropriate management of patients with the new onset RBBB during cardiac ischemia can have a significant impact on cardiac function and outcomes. In this series, we present four cases of new-onset acute RBBB associated with chest pain in the setting of acute myocardial infarction with critical lesions of the left anterior descending artery. We also highlight the need to consider new RBBB as an additional indication for acute reperfusion therapy in acute myocardial infarction. This will call for revision in the current guidelines by American Heart Association following the initiative recently implemented by the European Society of Cardiology 2018.
Background Few therapies exist to treat severe COVID-19 respiratory failure once it develops. Given known diffuse pulmonary microthrombi on autopsy studies of COVID-19 patients, we hypothesized that tissue plasminogen activator (tPA) may improve pulmonary function in COVID-19 respiratory failure. Methods A multicenter, retrospective, observational study of patients with confirmed COVID-19 and severe respiratory failure who received systemic tPA (alteplase) was performed. Seventy-nine adults from seven medical centers were included in the final analysis after institutional review boards' approval; 23 were excluded from analysis because tPA was administered for pulmonary macroembolism or deep venous thrombosis. The primary outcome was improvement in the PaO2/FiO2 ratio from baseline to 48 h after tPA. Linear mixed modeling was used for analysis. Results tPA was associated with significant PaO2/FiO2 improvement at 48 h (estimated paired difference = 23.1 ± 6.7), which was sustained at 72 h (interaction term p < 0.00). tPA administration was also associated with improved National Early Warning Score 2 scores at 24, 48, and 72 h after receiving tPA (interaction term p = 0.00). D-dimer was significantly elevated immediately after tPA, consistent with lysis of formed clot. Patients with declining respiratory status preceding tPA administration had more marked improvement in PaO2/FiO2 ratios than those who had poor but stable (not declining) respiratory status. There was one intracranial hemorrhage, which occurred within 24 h following tPA administration. Conclusions These data suggest tPA is associated with significant improvement in pulmonary function in severe COVID-19 respiratory failure, especially in patients whose pulmonary function is in decline, and has an acceptable safety profile in this patient population.
Cardiovascular disease (CVD) is the number one cause of death globally, accounting for 31% of all deaths in the world, and one out of every three deaths in the United States, in 2017 [1]. It is estimated that 90% of CVD is preventable, with traditional risk factors including tobacco use, excessive alcohol consumption, and unhealthy diet and physical inactivity, leading to hypertension, diabetes, dyslipidemia, and obesity. The epidemic of obesity has increased over the past decade, affecting an estimated 37.7% of adults, and 18% of children, in the US, and projected to rise to 51% of the population, a 130% increase, by 2030 [2]. This obesity epidemic has ushered in a new, highly prevalent, but largely underdiagnosed CVD risk factor: obstructive sleep apnea (OSA). OSA affects 34% of men, and 17% of women in the United States [3]. It is characterized by repetitive episodes of hypoventilation and complete apnea during sleep caused by total pharyngeal collapse and airway obstruction, despite normal breathing effort and drive. OSA’s impact on CVD appears to be due to recurrent cardio metabolic perturbations experienced when repetitively attempting to breath against an occluded airway, precipitating nightly episodes of hypoxia, sleep disturbance, and sympathetic nervous system surges, culminating in elevated blood pressure and heart rate, endothelial dysfunction, systemic inflammation and insulin resistance-all mechanisms involved in the pathogenesis of CVD (Figure 1) [4]. Accumulating evidence has linked OSA to multiple cardiovascular disorders including hypertension, type 2 DM, coronary artery disease, heart failure and cardiac arrhythmias (Figure 2).
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Figure 1
Pathophysiological mechanisms linking obstructive sleep apnea to cardiovascular disease.
A 62-year-old woman presents for pulmonary vein isolation (PVI) for paroxysmal atrial fibrillation. During transseptal catheterization (TSC) the patient sustained mechanical injury to the atrioventricular node (AVN) with consequent complete heart block (CHB). Injury to the AVN and CHB recovered after approximately forty minutes. The patient subsequently underwent a successful PVI with the remainder of the hospital stay uneventful. We present a case of reversible injury to the AVN caused by a steerable introducer sheath during TSC and discuss the mechanisms of injury as well as potential measures to avoid such a complication in the future.
Echocardiography was performed on 9 patients being treated for cardiogenic shock with an intra-aortic balloon. The value of simultaneous recording of the electrocardiogram, cardiac movements, and arterial pressure, with the echocardiogram of the intra-aortic balloon is discussed. The results indicate that echocardiography provides a method of studying intra-aortic balloon function.
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