Since the onset of the global pandemic in early 2020, coronavirus disease 2019 (COVID-19) has posed a multitude of challenges to health care systems worldwide. In order to combat these challenges and devise appropriate therapeutic strategies, it becomes of paramount importance to elucidate the pathophysiology of this illness. Coronavirus disease 2019, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), is characterized by a dysregulated immune system and hypercoagulability. COVID-associated coagulopathy (CAC) was recognized based on profound d-dimer elevations and evidence of microthrombi and macrothrombi, both in venous and arterial systems. The underlying mechanisms associated with CAC have been suggested, but not clearly defined. The model of immunothrombosis illustrates the elaborate crosstalk between the innate immune system and coagulation. The rendering of a procoagulant state in COVID-19 involves the interplay of many innate immune pathways. The SARS-CoV2 virus can directly infect immune and endothelial cells, leading to endothelial injury and dysregulation of the immune system. Activated leukocytes potentiate a procoagulant state via release of intravascular tissue factor, platelet activation, NETosis, and inhibition of anticoagulant mechanisms. Additional pathways of specific relevance in CAC include cytokine release and complement activation. All these mechanisms have recently been reported in COVID-19. Immunothrombosis provides a comprehensive perspective of the several synergistic pathways pertinent to the pathogenesis of CAC.

With increasing legalization, marijuana has become the most commonly abused substance in the United States. Together with the introduction of more potent marijuana products over the years, more adverse events are being reported and clinically characterized. Delta-9-tetrahydrocannabinol (THC) is the active psychotropic component of marijuana, which acts mainly on G-protein cannabinoid receptors CB1 and CB2. Multiple isolated cases of arrhythmias associated with marijuana use have been published. In this manuscript we conduct a scoping study of a total of 27 cases of arrhythmia associated with marijuana. Most cases were reported in young males (81%) with a mean age of 28 ± 10.6 years. Atrial fibrillation (26%) and ventricular fibrillation (22%) were the most common arrhythmias reported. Brugada pattern was reported in 19% of the patients. Marijuana associated arrhythmia resulted in a high mortality rate of 11 %. While the exact mechanisms of arrhythmias associated with marijuana are not clear, several hypothesis have been introduced including the effect of marijuana on cardiac ion channels as well as its effects on the central nervous system. In this paper we discuss the possible mechanisms of marijuana induced arrhythmia citing the evidence available to-date.

Background: Obesity is a growing pandemic that is associated with multiple cardiovascular disease (CVD) risk factors such as hypertension, diabetes, dyslipidemia and obstructive sleep apnea. With the increase in obesity rates where nearly two thirds of Americans are either obese or overweight, there has been an increase in the use of pharmacological therapy weight loss. While these therapies have shown benefit in weight reduction, the clinical impact these pharmacological agents on overall CVD outcomes has yet to be determined. Aim: We aimed to assess the effect of pharmacological agents used for weight reduction on CVD risk and all-cause mortality. Methods: We conducted a meta-analysis of peer-reviewed literature that evaluated the impact of anti-obesity drugs on cardiovascular outcomes. Key words used included: “orlistat”, “lorcaserin”, “phentermine/topiramate” or “naltrexone/bupropion” and “cardiovascular outcomes” among others. We reviewed 791 articles, only 47 studies were randomized controlled trials and only 7 studies fulfilled all the inclusion criteria including, quantitative data on cardiovascular risk factors such as, Hemoglobin A1C (A1C), changes in body mass index (BMI), blood pressure and CVD morbidity and mortality. Data was retrieved from these studies and evaluated with comprehensive meta-analysis software® to assess pooled effects for medical management versus placebo. Results: There were 7 studies included in the final analysis, with a total of 18,598 subjects, of which 8,685 were in the intervention (INT) group and 9,913 in the control (CTRL) group. For all cause mortality, there were 45 events in the INT and 55 in the CTRL groups, suggesting no significant difference between the two groups (OR: 0.843, 95%CI: 0.571–1.244, Z: −0.860, P: 0.390). For CVD mortality, there were 17 events in the INT and 36 events in the CTRL groups suggesting a significant mortality benefit in the INT group (OR:0.496, 95% CI: 0.282–0.873, Z: −2.433, P: 0.015). There was a significant absolute reduction in A1C in the INT group (Hg: −0.238, 95%CI: −0.291 to −0.186, Z: −8.937, P< 0.001). The percentage weight reduction was significantly higher for the INT group compared to the CTRL group (Hg: −0.431, 95%CI: −0.477 to −0.385, Z: −18.472, P< 0.001) and the blood pressure reduction was higher for the INT group compared to the CTRL group. (Hg: −0.052, 95%CI: −0.101- −0.003, Z: −2.086, P: 0.037). The heterogeneity observed for our meta analysis is Q: 1.884, df: 6, P: 0.930. Conclusions: Our study demonstrated the favorable and significant effect of pharmacological weight reduction strategies on weight loss, blood pressure reduction, glycemic control (A1C reduction), and CVD mortality. While weight loss without pharmacological means has been shown to reduce CVD risk, the mechanism by which weight loss medications impact CVD risk reduction could be a direct effect of these agents or merely an effect of weight reduction itself. Weight loss has been noted to modify risk factors via improving insulin sensitivity, reduci...

Takotsubo Cardiomyopathy is a syndrome characterized by transient and reversible regional myocardial dysfunction in the absence of obstructive coronary artery disease classically resulting in ventricular apical ballooning. It has a strong female predominance with onset generally in seventh decade of life, with hypothesized pathophysiology related to excess of catecholaminergic stimulation, particularly during episodes of physical or emotional stress. Takotsubo cardiomyopathy has been previously reported during myasthenic crisis, the acute deterioration of myasthenia gravis typically involving respiratory failure that is also associated with physical or emotional stress. We present the case of an atypically young male patient with classical takotsubo cardiomyopathy in the setting of myasthenic crisis after thymectomy initially concerning for ST segment elevation myocardial infarction, and a review of the literature of takotsubo cardiomyopathy in myasthenic crisis.

Marijuana abuse is rapidly growing and currently it is the most coimnon drug of abuse in the United States due to increased legalization for recreational and medicinal use. Delta 9-tetrahydrocannibol, the main psychoactive compound in marijuana, acts via the endocannabinoid system to elicit various cardiovascular physiological effects, and has been associated with many adverse cardiovascular effects such as acute coronary syndrome, arrhythmias, and sudden cardiac death that have previously been reported by our group and others. We present a case of a 30-year-old African-American male with no cardiovascular disease (CVD) risk factors with recurrent ST-segment elevation myocardial infarctions (STEMI) whose coronary angiography revealed recurrent 100% occlusion of the left anterior descending artery (LAD) in the setting of marijuana smoking. It was the patient’s third STEMI with 100% occlusion of the LAD with each STEMI secondary to thrombosis of a different region of the LAD. Marijuana use was confirmed by urine toxicology screening at each STEMI presentation. Coronary angiography on multiple occasions was negative for stenosis of other epicardial coronary arteries, and coronary calcimn scoring was zero. Evaluation for other cardiovascular risk factors including family history of premature coronary artery disease, dyslipidemia, diabetes, and hypercoagulable disorders was negative. Further studies are required to elucidate the mechanisms of marijuana-associated coronary thrombosis and myocardial infarction.

Mesothelioma is a rare tumor of the pleura, peritoneum, pericardium or tunica vaginalis. About 2,500 cases are diagnosed annually in the United States. Mesothelioma often presents with pleuritic chest pain and dyspnea related to local invasion; distal metastasis and lymphadenopathy at the time of diagnosis is rare. Pericardial involvement in mesothelioma is related to direct invasion of the tumor. We here present a 71 year-old-male who presented with pleuritic chest pain and dyspnea, noted to have diffuse ST-segment elevation in EKG and cardiac tamponade physiology on 2D echocardiogram in who imaging subsequently revealed left upper lung mesothelioma. A pericardial window was created following which tamponade resolved. The pericardial biopsy did not show any mesothelioma cells or fibrous plaques. Computer tomography revealed regional lymphadenopathy in the chest. Disrupted cardiac lymphatic flow due to tumor mesothelioma induced lymphadenopathy is likely cause of the cardiac tamponade in this patient. This is the second ever reported case of pleural mesothelioma without a direct pericardial invasion that presented with cardiac tamponade.

Background: The 'Spiked Helmet' is an electrocardiogram (EKG) finding occasionally seen in critically ill patients characterized by ST segment elevation usually represented as a 'spike and dome' pattern with elevation in the EKG baseline prior to the R wave and adjoining ST segment elevation resembling the German military helmet of the Prussian Empire. In the few cases reported in literature, this finding has been associated with very poor clinical outcomes, including in-hospital death. Although ST elevation is not uncommon in critically ill patients, these findings of a 'Spiked Helmet' sign are often transient and typically not associated with acute coronary syndrome. Case presentation: A 56-year-old male was found unresponsive by his relatives at home. It was an unknown the time that he had been unconscious. When the emergency medical services arrived, patient was found to be in pulseless electrical activity (PEA). Patient achieved return to spontaneous circulation (ROSC) 15 minutes after initiation of advanced cardiac life support protocol. An electrocardiogram done immediately post ROSC showed ST elevations in inferior and lateral leads. Patient was brought to the hospital as a ST elevated myocardial infarction (STEMI) arrest. The EKG revealed the Helmet sign in leads aVL and II, also ST segment elevation was noted in V1, V2, V3 and ST segment depression was noted in V5 and V6. Troponin was negative at the time of initial evaluation but trended up gradually during the hospitalization. A computed tomography (CT) pulmonary angiogram was negative for pulmonary embolism. A head CT showed diffuse anoxic brain injury. Patient was started on the hypothermia protocol. Upon family request patient was terminally extubated two days into hospital stay and expired shortly after. Conclusion: Although we are yet to fully understand the significance of the 'Spiked Helmet' Sign, this case report and literature review offers a comprehensive overview of the reported cases and draws important links and clues from them.

Contrast media enhances the visualization of the anatomic structures in radiological studies, allowing internal tissues such as blood vessels, kidney, ureters, adrenals and other organs to be identified. The evolution of contrast media highlights the efforts to develop less toxic chemical agents that possess low viscosity and osmolality. However, adverse effects such as idiosyncratic reactions, and organ specific damage are well characterized. Neurotoxicity, an important and dose related effect, appears to be due to disruption of the blood-brain-barrier by the high osmolarity of the contrast agent. From devastating cortical blindness to paralysis and seizures, an array of neurological manifestations has been described. In this systematic review, we describe the contrast-induced neurologic injury following coronary angiography and discuss the proposed mechanisms of injury leading to neurotoxicity.