Current cardiology reports
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To briefly review epidemiology and pathophysiology of SICM and provide a more extensive review of the data on diagnostic and management strategies. ⋯ SICM is likely underdiagnosed and that has mortality implications. Current evidence supports speckle tracking echocardiography to identify decreased contractility irrespective of left ventricular ejection fraction for the diagnosis of SICM. There continues to be a dearth of large clinical trials evaluating the treatment of SICM and current consensus focuses on supportive measures such as vasopressors and inotropes. Sepsis is a significant cause of mortality, and sepsis-induced cardiomyopathy has both prognostic and management implications for these patients. Individualized work-up and management of these patients is crucial to improving outcomes.
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Coronavirus disease of 2019 (COVID-19) is a cause of significant morbidity and mortality worldwide. While cardiac injury has been demonstrated in critically ill COVID-19 patients, the mechanism of injury remains unclear. Here, we review our current knowledge of the biology of SARS-CoV-2 and the potential mechanisms of myocardial injury due to viral toxicities and host immune responses. ⋯ A number of studies have reported an epidemiological association between history of cardiac disease and worsened outcome during COVID infection. Development of new onset myocardial injury during COVID-19 also increases mortality. While limited data exist, potential mechanisms of cardiac injury include direct viral entry through the angiotensin-converting enzyme 2 (ACE2) receptor and toxicity in host cells, hypoxia-related myocyte injury, and immune-mediated cytokine release syndrome. Potential treatments for reducing viral infection and excessive immune responses are also discussed. COVID patients with cardiac disease history or acquire new cardiac injury are at an increased risk for in-hospital morbidity and mortality. More studies are needed to address the mechanism of cardiotoxicity and the treatments that can minimize permanent damage to the cardiovascular system.
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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the virus responsible for the aggressive coronavirus disease (COVID-19) pandemic. Recently, investigators have stipulated that COVID-19 patients receiving angiotensin-converting-enzyme inhibitors (ACEI) may be subject to poorer outcomes. This editorial presents the available evidence to guide treatment practices during this pandemic. ⋯ Recent studies from Wuhan cohorts provide valuable information about COVID-19. A cohort with 52 critically ill patients revealed cardiac injury in 12% of patients. Worse outcomes appear to be more prevalent in patients with hypertension and diabetes mellitus (DM), possibly due to overexpression of angiotensin-converting enzyme 2 (ACE2) receptor in airway alveolar epithelial cells. Investigators suspect that SARS-CoV-2 uses the ACE2 receptor to enter the lungs in a mechanism similar to SARS-CoV. Several hypotheses have been proposed to date regarding the net effect of ACEI/ARB on COVID-19 infections. Positive effects include ACE2 receptor blockade, disabling viral entry into the heart and lungs, and an overall decrease in inflammation secondary to ACEI/ARB. Negative effects include a possible retrograde feedback mechanism, by which ACE2 receptors are upregulated. Even though physiological models of SARS-CoV infection show a theoretical benefit of ACEI/ARB, these findings cannot be extrapolated to SARS-CoV-2 causing COVID-19. Major cardiology scientific associations, including ACC, HFSA, AHA, and ESC Hypertension Council, have rejected these correlation hypotheses. After an extensive literature review, we conclude that there is no significant evidence to support an association for now, but given the rapid evolvement of this pandemic, findings may change.
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The total artificial heart (TAH) is a form of mechanical circulatory support that involves resection of the native ventricles followed by placement of a device that can restore total pulmonary and systemic flow. Given the increasing burden of congestive heart failure and cardiovascular disease, the number of people in need of cardiac replacement therapy will continue to grow. Despite aggressive efforts to expand the donor pool, the number of heart transplants in the United States (US) has plateaued at less than 3000 per year. ⋯ Current LVADs are associated with significant long-term complications related to retention of the native heart and pump design. Many of these complications may be addressed by the increased use of cardiac replacement therapy, i.e., total artificial hearts. Multiple generations of both pulsatile and advanced design continuous flow TAH are under development which have the potential to expand the role of TAHs.
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To review the clinical evidence for a relationship between obstructive sleep apnea and hypertension, arrhythmias, coronary artery disease, and congestive heart failure. ⋯ Current data show that obstructive sleep apnea is a risk for cardiovascular disease. Studies have linked untreated moderate to severe obstructive sleep apnea to hypertension, cardiac arrhythmias, coronary artery disease, and congestive heart failure. However, uncertainty regarding benefits of treatment of obstructive sleep apnea to reduce the risk of cardiovascular disease still exists. The issue of poor compliance has been an on-going limitation of CPAP trials. Evidence shows obstructive sleep apnea is a risk factor for cardiovascular disease but trials have yet to clarify if cardiovascular disease morbidity and mortality decreases with treatment of the apnea. Future treatment trials are needed to address the question of whether treatment decreases cardiovascular risk in patients with obstructive sleep apnea.