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BackgroundTreatment with phosphodiesterase type 5 inhibitors (PDE-5is) is effective in treating erectile dysfunction (ED).AimThe objective of this study was to determine the effect of PDE-5is on the incidence of major adverse cardiovascular (CV) events (MACE; composite outcome of CV death, hospitalization for myocardial infarction, coronary revascularization, stroke, heart failure, and unstable angina pectoris) and overall mortality.MethodsA retrospective observational cohort study was conducted in a large US claims database in men with ≥1 diagnosis of ED without prior MACE within 1 year, from January 1, 2006, to October 31, 2020. The exposed group had ≥1 claim for PDE-5i and the unexposed group had no claims for PDE-5i, and the groups were matched up to 1:4 on baseline risk variables.OutcomeThe primary outcome was MACE and the secondary outcomes were overall mortality and individual components of MACE, determined by multivariable Cox proportional hazard modeling.ResultsMatched plus multivariable analyses showed that MACE was lower by 13% in men exposed (n = 23 816) to PDE-5is (hazard ratio [HR] 0.87; 95% CI 0.79-0.95; P = .001) vs nonexposure (n = 48 682) over mean follow-up periods of 37 and 29 months, respectively, with lower incidence of coronary revascularization (HR 0.85; 95% CI 0.73-0.98; P = .029), heart failure (HR 0.83; 95% CI 0.72-0.97; P = .016), unstable angina (HR 0.78; 95% CI 0.64-0.96; P = .021), and CV death (HR 0.61; 95% CI 0.41-0.90; P = .014) with PDE-5i exposure. Phosphodiesterase type 5 inhibitor–exposed men had a 25% lower incidence of overall mortality (HR 0.75; 95% CI 0.65-0.87; P Clinical ImplicationsPDE-5is may have cardioprotective effects.Strengths and LimitationsStrengths are the large numbers of participants and consistency of the data; limitations include the retrospective nature of the study and unknown confounders.ConclusionsIn a large population of US men with ED, PDE-5i exposure was associated with lower incidence of MACE, CV death, and overall mortality risk compared to non-exposure. Risk reduction correlated with PDE-5i exposure level.

BackgroundElectronic cigarettes (eC) may not be entirely benign. There is a lack of data on the effect of a single acute exposure of eC vapor using various heating sources and power settings upon lung injury. The purpose of this study was to determine if an acute exposure with eC vapor heated with different heating elements and power levels induced inflammatory changes in the lungs and heart.MethodsRats were exposed to pure air or received a single, 4-h exposure to eC vapor. The devices used either a stainless steel (SS) or nichrome (NC) heating element randomized to a low or high atomization power (45 versus 70 W). Rats were euthanized within 48 h of exposure.ResultsThe eC groups showed accumulation of inflammatory cells in bronchial lumen, near the pleura, and within the alveolar spaces. The numbers of inflammatory cells per field in the lung parenchyma were significantly greater in the rats exposed to eC groups vs. the air group. There were significantly higher inflammatory gene expression changes in the lungs of animals assigned to 70 W power. We observed that eC vapor generated using burnt coils were toxic and could cause acute respiratory distress and myocarditis.ConclusionIn conclusion, one 4-h exposure to eC vapor, in the absence of vitamin E oil or nicotine, significantly increased lung inflammation. Effects were seen after exposures to vapor generated using SS and NC heating elements at either high or low power. Vapor from devices with burnt coils can negatively affect the heart and lung.

Summary Despite the fact that door-to-balloon times have been greatly reduced, the rates of death and the incidence of heart failure in patients with ST-segment elevation myocardial infarction (MI) have plateaued. There is still an unmet need to further reduce MI size in the reperfusion era. Most adjunctive therapies to enhance myocardial salvage have failed, but some have shown promise. Currently, the only adjunctive therapy in a pivotal trial that has demonstrated reductions in infarct size is localized delivery of supersaturated oxygen (SSO2) therapy. This review provides background on prior infarct size reduction efforts. The authors describe the preclinical data that shows the effectiveness of SSO2 in reducing MI size, improving regional myocardial blood flow and cardiac function, and reducing adverse left ventricular remodeling—presumably by reducing patchy areas of residual ischemia within the reperfused risk zone. Potential mechanisms by which SSO2 is beneficial are described, including the delivery of high levels of dissolved oxygen through plasma to ischemic, but viable, vascular and myocardial cells, thus allowing their survival and function. The authors then describe the SSO2 clinical trials, demonstrating that in patients with anterior ST-segment elevation MI, SSO2 therapy safely and effectively reduces infarct size, improves cardiac function, and reduces adverse left ventricular remodeling.

Viral diseases are some of the most common infections affecting humans. Despite the unpleasant symptoms, most people return to their normal lives without residual symptoms. Following the acute infectious phase of some viruses, however, in some individuals symptoms may linger to the extent they are unable to return to a normal lifestyle. Following coronavirus disease 2019 infection, significant numbers of patients continued to have symptoms that persisted for months after hospital discharge. Symptoms spanned many organ systems and were prominent in the pulmonary and cardiovascular systems. The exact mechanism is not clear. This group of patients represents a new challenge to our health care systems. An organized, multi-disciplinary approach and further research are warranted to be ready to deliver better care to these patients.

Item does not contain fulltext Cardiac MRI is a noninvasive diagnostic tool using nonionizing radiation that is widely used in patients with ST-segment elevation myocardial infarction (STEMI). Cardiac MRI depicts different prognosticating components of myocardial damage such as edema, intramyocardial hemorrhage (IMH), microvascular obstruction (MVO), and fibrosis. But how do cardiac MRI findings correlate to histologic findings? Shortly after STEMI, T2-weighted imaging and T2* mapping cardiac MRI depict, respectively, edema and IMH. The acute infarct size can be determined with late gadolinium enhancement (LGE) cardiac MRI. T2-weighted MRI should not be used for area-at-risk delineation because T2 values change dynamically over the first few days after STEMI and the severity of T2 abnormalities can be modulated with treatment. Furthermore, LGE cardiac MRI is the most accurate method to visualize MVO, which is characterized by hemorrhage, microvascular injury, and necrosis in histologic samples. In the chronic setting post-STEMI, LGE cardiac MRI is best used to detect replacement fibrosis (ie, final infarct size after injury healing). Finally, native T1 mapping has recently emerged as a contrast material-free method to measure infarct size that, however, remains inferior to LGE cardiac MRI. Especially LGE cardiac MRI-defined infarct size and the presence and extent of MVO may be used to monitor the effect of new therapeutic interventions in the treatment of reperfusion injury and infarct size reduction. © RSNA, 2021 Online supplemental material is available for this article.

COVID-19 has had significant secondary effects on health care systems, including effects on emergency medical services (EMS) responses for time-sensitive emergencies. We evaluated the correlation between COVID-19 hospitalizations and EMS responses for time-sensitive emergencies in a large EMS system. This was a retrospective study using data from the Los Angeles County EMS Agency. We abstracted data on EMS encounters for stroke, ST-elevation myocardial infarction (STEMI), out-of-hospital cardiac arrest (OHCA), and trauma from April 5, 2020 to March 6, 2021 and for the same time period in the preceding year. We also abstracted daily hospital admissions and censuses (total and intensive care unit [ICU]) for COVID-19 patients. We designated November 29, 2020 to February 27, 2021 as the period of surge. We calculated Spearman’s correlations between the weekly averages of daily hospital admissions and census and EMS responses overall and for stroke, STEMI, OHCA, and trauma. During the study period, there were 70,616 patients admitted for confirmed COVID-19, including 12,467 (17.7%) patients admitted to the ICU. EMS responded to 899,794 calls, including 9,944 (1.1%) responses for stroke, 3,325 (0.4%) for STEMI, 11,207 (1.2%) for OHCA, and 114,846 (12.8%) for trauma. There was a significant correlation between total hospital COVID-19 positive patient admissions and EMS responses for all time-sensitive emergencies, including a positive correlation with stroke (0.41), STEMI (0.37), OHCA (0.78), and overall EMS responses (0.37); and a negative correlation with EMS responses for trauma (-0.48). ICU COVID-19 positive patient admissions also correlated with increases in EMS responses for stroke (0.39), STEMI (0.39), and OHCA (0.81); and decreased for trauma (-0.53). Similar though slightly weaker correlations were found when evaluating inpatient census. During the period of surge, the correlation with overall EMS responses increased substantially (0.88) and was very strong with OHCA (0.95). We found significant correlation between COVID-19 hospitalizations and the frequency of EMS responses for time-sensitive emergencies in this regional EMS system. EMS systems should consider the potential effects of this and future pandemics on EMS responses and prepare to meet non-pandemic resource needs during periods of surge, particularly for time-sensitive conditions.

Purpose : The present study was to determine whether OP2113 could limit myocardial infarction size and the no-reflow phenomenon in a rat myocardial ischemia/reperfusion model. Methods : Rat heart–isolated mitochondria (RHM) were used to investigate mitochondrial respiration and mitochondrial reactive oxygen species (mtROS) generation both in normal conditions and in ischemia/reperfusion-mimicking conditions (using high concentrations of succinate). Human skeletal muscle myoblasts (HSMM) in culture were used to investigate the cellular intermittent deprivation in energy substrates and oxygen as reported in ischemia/reperfusion conditions. In vivo, rats were anesthetized and subjected to 30 min of left coronary artery occlusion followed by 3 h of reperfusion. Rats were randomized to receive OP2113 as an intravenous infusion starting either 5 min prior to coronary artery occlusion (preventive), or 5 min prior to reperfusion (curative), or to receive vehicle starting 5 min prior to coronary artery occlusion. Infusions continued until the end of the study (3 h of reperfusion). Results : RHM treated with OP2113 showed a concentration-dependent reduction of succinate-induced mtROS generation. In HSMM cells, OP2113 treatment (5–10 μM) during 48H prevented the reduction in the steady-state level of ATP measured just after reperfusion injuries and decreased the mitochondrial affinity to oxygen. In vivo, myocardial infarct size, expressed as the percentage of the ischemic risk zone, was significantly lower in the OP2113-treated preventive group (44.5 ± 2.9%) versus that in the vehicle group (57.0 ± 3.6%; p

First documented in China in early December 2019, the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spread rapidly and continues to test the strength of healthcare systems and public health programs all over the world. Underlying cardiovascular disease has been recognized as a risk factor for coronavirus disease 2019 (COVID-19)-related morbidity and mortality since the early days of the pandemic. In addition, evidence demonstrates cardiac and endothelial damage in somewhere between one-third and three-quarters of individuals with COVID-19, regardless of symptom severity. This damage is thought to be mediated by direct viral infection, immunopathology and hypoxemia with the additional possibility of exacerbation via medication-induced cardiotoxicity. Clinically, the cardiovascular consequences of COVID-19 may present as myocarditis with or without arrhythmia, endothelial dysfunction and thrombosis, acute coronary syndromes and heart failure. Presentation can vary widely and may or may not be typical of the condition in an individual without COVID-19. There is evidence to support the prognostic utility of cardiac biomarkers (e.g., cardiac troponin) and imaging studies (e.g., echocardiography, cardiac magnetic resonance imaging) in the context of COVID-19 and building evidence suggests that cardiovascular screening may be warranted even among those with asymptomatic or mild infection and those without traditional cardiovascular risk factors. In addition, evidence suggests the potential for long-term cardiovascular consequences for those who recover from COVID-19 with implications for the field of cardiology long into the future. Even among those without COVID-19, disruption of infrastructure and changes in human behavior as a result of the pandemic also have an upstream role in cardiovascular outcomes, which have already been documented in multiple locations. This review summarizes what is currently known regarding the pathogenic mechanisms of COVID-19-related cardiovascular injury and describes clinical cardiovascular presentations, prognostic indicators, recommendations for screening and treatment, and long-term cardiovascular consequences of infection. Ultimately, medical personnel must be vigilant in their attention to possible cardiovascular symptoms, take appropriate steps for clinical diagnosis and be prepared for long-term ramifications of myocardial injury sustained as a result of COVID-19.

Background: Phosphodiesterase type 5 inhibitor (PDE-5i) medications are effective in treating Erectile Dysfunction (ED) for tens of millions of men in the US and worldwide. The objective of this study was to determine the effect of PDE-5is on the incidence of major adverse cardiovascular events (MACE) (composite outcome of cardiovascular (CV) death, hospitalization for myocardial infarction, coronary revascularization, stroke, heart failure, or unstable angina pectoris) and all-cause death. Methods: A retrospective observational cohort study was conducted in a large US commercial and Medicare insurance claims database in men with ≥1 diagnosis of ED without prior MACE hospitalization within 1 year from Jan 2006 to Oct 2020. The exposed group had ≥1 claim for PDE-5i; the unexposed group had no claims for PDE-5i and were matched 2:1 on baseline risk variables. The primary outcome was MACE and secondary outcome was all-cause death, determined by multivariate Cox proportional hazard modeling. Death data were obtained via National Death Index linkage. Results: In this population, MACE was reduced by 13% in men exposed (n=23,816) to PDE-5is (hazard ratio (HR) 0.87; 95% Confidence Interval (CI) 0.79-0.95) vs. non-exposure (n=48,682) over mean follow up of 29 and 37 months, respectively. This was driven by reductions in coronary revascularization (HR 0.85; 0.73-0.98), heart failure (HR 0.83; 0.72-0.97), unstable angina (HR 0.78; 0.64-0.96), and CV death (HR 0.61; 0.41-0.90). PDE-5i-exposed men had a 25% reduction in all-cause death (HR 0.75; 0.65-0.87). Men without coronary artery disease but with CV risk factors at baseline showed a similar pattern. In the main study cohort, men in the highest quartile of PDE-5i exposure had the greatest reductions in MACE (HR 0.45; 0.37-0.54) and all-cause death (HR 0.51; 0.37-0.71) vs. the lowest exposure quartile. In a subgroup with baseline type 2 diabetes (n=6,305), PDE-5i exposure was associated with a lower MACE risk (HR 0.79; 0.64-0.97). All comparisons are significant at p Conclusions: In a large population of US men with ED, PDE-5i exposure was associated with reductions in MACE, CV death, and overall death risk compared to non-exposure. Risk reduction was positively correlated with PDE-5i exposure level.

We tested the hypothesis that therapeutic hypothermia (TH) improves survival and blunts inflammation in rats undergoing experimental hemorrhagic shock. Rats were randomized to TH (n = 16) or normot...

Electroencephalographic (EEG) alpha oscillations have been related to heart rate variability (HRV) and both change in Alzheimer's disease (AD). We explored if task switching reveals altered alpha power and HRV in cognitively healthy individuals with AD pathology in cerebrospinal fluid (CSF) and whether HRV improves the AD pathology classification by alpha power alone. We compared low and high alpha event-related desynchronization (ERD) and HRV parameters during task switch testing between two groups of cognitively healthy participants classified by CSF amyloid/tau ratio: normal (CH-NAT, n=19) or pathological (CH-PAT, n=27). For the task switching paradigm, participants were required to name the color or word for each colored word stimulus, with two sequential stimuli per trial. Trials include color (cC) or word (wW) repeats with low load repeating, and word (cW) or color switch (wC) for high load switching. HRV was assessed for RR interval, standard deviation of RR-intervals (SDNN) and root mean squared successive differences (RMSSD) in time domain, and low frequency (LF), high frequency (HF), and LF/HF ratio in frequency domain. Results showed that CH-PATs compared to CH-NATs presented: 1) increased (less negative) low alpha ERD during low load repeat trials and lower word switch cost (low alpha: p=0.008, Cohen's d=-0.83, 95% confidence interval -1.44 to -0.22, and high alpha: p=0.019, Cohen's d=-0.73, 95% confidence interval -1.34 to -0.13); 2) decreasing HRV from rest to task, suggesting hyper-activated sympatho-vagal responses. 3) CH-PATs classification by alpha ERD was improved by supplementing HRV signatures, supporting a potentially compromised brain-heart interoceptive regulation in CH-PATs. Further experiments are needed to validate these findings for clinical significance.

Introduction: It is important that physicians and patients are aware of the cardiovascular safety of options available to treat erectile dysfunction (ED)/benign prostatic hyperplasia (BPH) while on concomitant antihypertensive medications (AHM). Objective: This integrated safety analysis assessed the incidence of hypotension-related treatment-emergent adverse events (TEAEs) and major adverse cardiovascular events (MACE) in patients with concomitant use of tadalafil and AHM. Methods: Data were integrated from seventy-two Phase II-IV studies conducted on patients with a diagnosis of ED and/or BPH. Studies were categorized as either All placebo-controlled studies or All studies. The incidences of hypotensive-related TEAEs and MACE were analyzed by indication; by use of concomitant AHM; and by the number of concomitant AHM. Results: A total of 15,030 and 22,825 patients were included in the analyses for All placebo-controlled studies and All studies, respectively. In the All placebo-controlled studies, the incidence of hypotension-related TEAEs and MACE was ranging between 0.6-1.5% and 0.0-1.0%, respectively, across all indications and use of AHM. Tadalafil was associated with an increase in hypotension-related TEAEs only in the ED as-needed category not receiving any concomitant AHM (p-value=0.0070); no difference was reported between placebo and tadalafil in all indication categories of patients receiving ≥1 AHM (p-value≥ 0.7386). Similarly, no differences (p-value≥ 0.2238) were observed in the incidence of MACE between tadalafil and placebo treatment groups, with or without concomitant use of AHM, and across all indication categories. In the All studies results were similar. Conclusion: The concomitant use of tadalafil alongside AHM did not increase the risk of hypotension-related TEAEs or MACE compared with AHM alone. Figure Odds ratio of incidences of hypotension-related TEAEs between placebo and tadalafil groups by number of concomitant AHM

Background: A new form of lung injury was described in electronic cigarette users beginning July 2019 with patients presenting with respiratory distress. The condition is known as E-cigarette (eC) or vaping product use associated lung injury or EVALI and was thought to be related to Vit E oils used to dilute cannabis. Whether a single acute exposure of eC smoke can induce lung injury has not been reported. The purpose of this study was to determine if such an acute exposure with eC smoke heated with different heating elements and power levels induced inflammatory changes in the lungs and heart. Methods: Rats were exposed to pure air or received a single, 4-hour exposure to eC vapor (50% propylene glycol, 50% vegetable glycerin; tobacco flavoring, n=16 in each group). The devices used either a stainless steel (SS) or nichrome (NC) heating element randomized to a low or high atomization power (45 versus 70 Watts). Rats were euthanized within 48 hours of exposure and hematoxylin and eosin stained lung and cardiac histology sections were assessed. Inflammatory cells were counted from 12 random areas per section at 10 х magnification. Results: The lung alveoli appeared normal in the air group (Figure, panel A); the eC groups using the SS or NC heating element with high or low power showed accumulation of inflammatory cells (mainly macrophages) in bronchial lumen (B), near the pleura (C), and within the alveolar spaces (D). The numbers of inflammatory cells per field in the lung parenchyma were significantly greater in the rats exposed to eC using SS or NC heating element compared to the air control group (P < 0.05, One way ANOVA, Tukey multiple comparison test; panel E). Cardiac tissue appeared normal with no evidence of inflammation. Conclusion: One 4-hour exposure to eC vapor, in the absence of vitamin E oil or nicotine, significantly increased the number of inflammatory cells in the lung. Effects were seen after exposures to vapor generated using SS and NC heating elements at either high or low power.

The coexistence of cardiovascular disease and erectile dysfunction is widespread, possibly owing to underlying endothelial dysfunction in both diseases. Millions of patients with cardiovascular disease are prescribed phosphodiesterase-5 (PDE5) inhibitors for the management of erectile dysfunction. Although the role of PDE5 inhibitors in erectile dysfunction therapy is well established, their effects on the cardiovascular system are unclear. Preclinical studies investigating the effect of PDE5 inhibitors on ischemia–reperfusion injury, pressure overload-induced hypertrophy, and chemotoxicity suggested a possible clinical role for each of these medications; however, attempts to translate these findings to the bedside have resulted in mixed outcomes. In this review, we explore the biologic preclinical effects of PDE5 inhibitors in mediating cardioprotection. We then examine clinical trials investigating PDE5 inhibition in patients with heart failure, coronary artery disease, and ventricular arrhythmias and discuss why the studies likely have yet to show positive results and efficacy with PDE5 inhibition despite no safety concerns.

Highlights • Beyond restoring myocardial perfusion, there is an unmet need to further reduce the size of myocardial infarctions; only 1 therapy is FDA-approved to specifically treat ischemic myocardium as an adjunct to reperfusion therapy. • Here, we present the basic science and clinical studies showing that treatment with supersaturated oxygen following mechanical reperfusion therapy in patients with large anterior myocardial infarctions improves myocardial perfusion and reduces infarct size. • Early clinical studies also show that supersaturated oxygen improves left ventricular function and reduces adverse left ventricular remodeling in patients with large anterior myocardial infarctions., Summary Despite the fact that door-to-balloon times have been greatly reduced, the rates of death and the incidence of heart failure in patients with ST-segment elevation myocardial infarction (MI) have plateaued. There is still an unmet need to further reduce MI size in the reperfusion era. Most adjunctive therapies to enhance myocardial salvage have failed, but some have shown promise. Currently, the only adjunctive therapy in a pivotal trial that has demonstrated reductions in infarct size is localized delivery of supersaturated oxygen (SSO2) therapy. This review provides background on prior infarct size reduction efforts. The authors describe the preclinical data that shows the effectiveness of SSO2 in reducing MI size, improving regional myocardial blood flow and cardiac function, and reducing adverse left ventricular remodeling—presumably by reducing patchy areas of residual ischemia within the reperfused risk zone. Potential mechanisms by which SSO2 is beneficial are described, including the delivery of high levels of dissolved oxygen through plasma to ischemic, but viable, vascular and myocardial cells, thus allowing their survival and function. The authors then describe the SSO2 clinical trials, demonstrating that in patients with anterior ST-segment elevation MI, SSO2 therapy safely and effectively reduces infarct size, improves cardiac function, and reduces adverse left ventricular remodeling., Central Illustration

More than four decades ago, the United States Surgeon General issued a warning regarding the medical problems of marijuana smoking, including cardiac toxicity. Since then, many reports have described atrial fibrillation, ventricular tachycardia, acute coronary syndromes, and cardiac arrest temporally related to marijuana use. The subjects were quite young, with no significant cardiovascular risk factors, with the only obvious trigger being marijuana use. Despite these strong signals, the drug is now legalized for recreational use in many states. We believe the time has come to conduct definitive studies about the safety of marijuana before this trend moves to the rest of the nation.

There is evidence that certain stressors can trigger cardiovascular events. Several studies have now demonstrated an increase in major adverse cardiac events associated with natural disasters such as an earthquake. The purpose of this paper is to review the literature on earthquakes and cardiovascular events. Reports from 13 major quakes were reported. Earthquakes have been associated with a number of cardiac events including sudden cardiac death, fatal myocardial infarction (MI), myocardial infarction, stress cardiomyopathy, heart failure, stroke, arrhythmias, hypertension and pulmonary embolism. Most reports were associated with earthquakes of magnitude 6.0 or greater. Cardiac events were reported within hours of the quakes. In some reports there was a sharp spike in cardiac events followed by a decrease; but in other quakes the increases in cardiac events lasted weeks, months and even years. There often was an association between the cardiac events and amount of personal property loss. The Great East Japan Earthquake was an unusual event in that it was associated with a major tsunami and cardiac events appeared worse in inundated areas due to flooding. Some but not all reports suggested more MIs associated with early morning earthquakes that woke up the population. Hospitals in earthquake-prone areas should consider developing plans for handling increases in myocardial infarctions and other cardiac events that are associated with earthquakes.

The purpose of the study was to determine whether late therapeutic hypothermia (LTH), administered after reperfusion, could prevent adverse left ventricular (LV) remodeling and improve cardiac function in the rat myocardial ischemia/reperfusion model.Rats were randomized to normothermia (n = 10) or LTH (initiated at 1 min after coronary artery reperfusion, n = 10) and subjected to 30 min of coronary occlusion followed by 6 weeks of reperfusion. Hypothermia was induced by pumping cold saline over the anterior surface of the LV until the temperature cooled to32 °C. In the normothermic group, the heart was bathed in saline at 38 °C.After 6 weeks of recovery, fractional shortening of the LV was comparable in the LTH (20.2 ± 0.6%) and normothermic group (20.0 ± 2.1%; p = 0.918). Postmortem LV volume (0.47 ± 0.04 ml in LTH and 0.44 ± 0.05 ml in normothermic group) and lung wet/dry weight ratio were similar in both groups. There were no significant differences in scar size, scar thickness, infarct expansion index, LV cavity or transmurality (%) between groups. This data contrasts with our previous study showing that hypothermia administered during the ischemic phase significantly reduced the scar size; decreased LV cavity, infarct expansion index and transmurality (%), and improved the scar thickness.LTH did not prevent adverse LV remodeling nor improve cardiac function in the rat myocardial ischemia/reperfusion model. To have a long term benefit on remodeling, hypothermia must be administered during the ischemic phase and not just the reperfusion phase.

Myocarditis is common during viral infection with cases described as early as the influenza pandemic of 1917, and the current COVID-19 pandemic is no exception. The hallmark is elevated troponin, which occurs in 36% of COVID patients, with electrocardiogram, echocardiogram, and cardiac magnetic resonance being valuable tools to assist in diagnosis. Cardiac inflammation may occur secondary to direct cardiac invasion with the virus, or to intense cytokine storm, often encountered during the course of the disease. Angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and judicious use of beta-blockers are beneficial in management of myocarditis. Corticosteroids may be avoided during the very early phase of viral replication, but can be of clear benefit in hospitalized, critically ill patients. Statins are beneficial to shorten the course of the disease and may decrease mortality.

E-cigarettes have surged in popularity over the last few years, particularly among youth and young adults. These battery-powered devices aerosolize e-liquids, comprised of propylene glycol and vegetable glycerin, typically with nicotine, flavors, and stabilizers/humectants. Although the use of combustible cigarettes is associated with several adverse health effects including multiple pulmonary and cardiovascular diseases, the effects of e-cigarettes on both short- and long-term health have only begun to be investigated. Given the recent increase in the popularity of e-cigarettes, there is an urgent need for studies to address their potential adverse health effects, particularly as many researchers have suggested that e-cigarettes may pose less of a health risk than traditional combustible cigarettes and should be used as nicotine replacements. This report is prepared for clinicians, researchers, and other health care providers to provide the current state of knowledge on how e-cigarette use might affect cardiopulmonary health, along with research gaps to be addressed in future studies.

Author(s): Arakaki, Xianghong; Hung, Shao‐Min; Wei, Ke; Tran, Thao; Arechavala, Rebecca Johnson; Kleinman, Michael T; Kloner, Robert; Fonteh, Alfred N; King, Kevin; Harrington, Michael G

Background: Recently, the clinical entity of EVALI (E-cigarette or vaping product use associated lung injury) was described and has similarities to COVID -19 pneumonia. We determined in a quantitative manner the inflammatory changes in the lungs associated with EVALI in a rodent model that does not include use of marijuana, vitamin E oil, or nicotine, which had been implicated as a cause. Methods: Adult Sprague Dawley rats were exposed to either pure air (n=5) or electronic cigarette (eC) vapor (propylene glycol/vegetable glycerin, tobacco flavoring) using a device with a nickel-chromium alloy (NC) heating element at 70 Watts (n=6) for 2 hours. The e-liquid did not contain nicotine, marijuana, or Vitamin E oil. Rats were euthanized within a few days of exposure and H&E-stained lung sections were assessed. Inflammatory cells were counted from 10 random areas per section at 20х magnification. Results: Alveolar structure appeared normal in the air group (Figure, panel C); the eC group using the NC heating element showed alveolar inflammation (D). The numbers of inflammatory cells per high power field in the lung parenchyma were significantly greater in the rats exposed to eC using NC heating element (67.5 ± 44.5) compared to the air group (6.7 ± 0.3; P < 0.001, Kruskal-Wallis test). The predominant cell type was mononuclear and secondary were neutrophils. Other features included accumulation of fibrin and inflammatory cells in the lumen of the trachea (A); thickened alveolar walls; and red blood cell congestion (D). Inflammation of the nasal passages was also observed (B). Exposure of rats to e cigarettes using a stainless steel heating element did not result in EVALI, and the amount of inflammatory cells was closer to air exposed rats (7.2± 0.4). Conclusion: Vaping using a nichrome heating element at high power leads to respiratory tract pathology and a significant increase in the number of inflammatory cells in the alveoli. EVALI occurred without marijuana, vitamin E oil or nicotine.

Introduction: Nicotine is a major bioactive component in tobacco cigarettes and electronic cigarettes. Despite the fact that smokers are at higher risk of experiencing an acute myocardial infarction (AMI), there are few studies that have examined the acute effects of nicotine on AMI.To address this issue, our present study was to examine the acute effects of nicotine on myocardial infarct size, no reflow, cardiac hemodynamics and cardiac function in a rat myocardial infarct model. Methods: Forty-six female Sprague-Dawley rats were randomly divided into nicotine group and control group (n=23/group) and received an intravenous loading dose of nicotine at 2.0 μg/kg/min or saline for 30 minutes before starting coronary artery occlusion, then followed by a maintenance dose 0.35 μg/kg/min of nicotine to the end of 3.5 hours of occlusion (30 minutes) and reperfusion (3 hours). Results: At baseline, there were no difference between the two study groups, in systolic blood pressure (BP in mmHg) (nicotine, 69.0±2.7; control, 69.3±4.4; p > 0.05), or diastolic BP (nicotine, 45.7±3.2; control, 48.2±4.2; p > 0.05). Nicotine initially increased systolic BP (nicotine, 97.0±8.6; control, 69.2±3.3, p p < 0.01) at 10 minutes after starting injection of the loading dose; pressures dropped to control levels in both groups at 30 minutes. During occlusion/reperfusion, the BP and heart rate were not altered by nicotine. Nicotine significantly increased myocardial infarct size as a percentage of the ischemic risk zone compared to the controls (nicotine, 54.9 ± 1.9 %; control, 48.6 ± 2.7 %, p < 0.05), but nicotine did not affect the no-reflow size (nicotine, 34.8 ± 3.10 %; control, 33.7 ± 3.0%, p > 0.05). Nicotine did not alter fractional shortening assessed by echocardiography. Conclusions: Nicotine infusion can transiently increase blood pressure in anesthetized rats. During coronary occlusion and reperfusion, nicotine increased myocardial infarct size, but did not affect hemodynamics or fractional shortening, suggesting that the increase in infarct size was not simply due to an increase in oxygen demand due to altered afterload, heart rate or contractility, but may reflect a more direct effect on the myocardium.

Background: We investigated the effects of chronic electronic cigarettes with nicotine (E-Cig) exposure on cardiovascular function in rats. Methods: Adult Sprague Dawley rats were exposed to either pure air (n=10) or E-Cig (n=14) for 12 weeks. After 12 weeks of exposure, flow-mediated vasodilation was measured in anesthetized rats with ultrasound to measure femoral artery diameter. Femoral artery flow velocity was measured before and 5 minutes after reperfusion of a 5-minute femoral artery occlusion. Cardiac function was assessed by echocardiogram. A Millar catheter was used to record systemic arterial and LV pressures. Cardiac output was measured using a themodilution catheter. Results: The femoral artery internal diameter and blood flow velocity were comparable between the 2 groups before and after artery occlusion. However, in the E-cig group, blood flow velocity significantly decreased from 55.5 ± 5.2 cm/s prior to occlusion to 41.3 ± 4.1 cm/s after reperfusion (p = 0.005); it remained similar prior to (47.8 ± 3.4 cm/s) and after (47.8 ± 5.5 cm/s) occlusion in the air group. There were no statistically significant differences in left ventricular diastolic and systolic dimensions, LV fractional shortening, heart rate or mean blood pressure (80 ± 3 mmHg in air and 79 ± 5 mmHg in E-cig group) , LV end-diastolic pressure (Ped), end-systolic pressure (Pes), peak -dP/dt, Tau, or cardiac output (48.3 ± 3.3 ml/min in air and 47.6 ± 3.9 ml/min in E-cig group) between the E-Cig and the pure air group. There was a trend toward a reduction in peak LV +dP /dt in the E-Cig group (5574 ± 341 mmHg/s) compared to the air group (6166 ± 238 mmHg/s). LV weight and wall thickness were similar between groups. Conclusions: Twelve weeks of E-Cig exposure did not affect heart rate or blood pressure; but did tend to reduce contractility. E-cigarette exposure slowed the flow-mediated blood flow velocity probably at a microvascular level, possibly by altering endothelial function.