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.
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.
Lacosamide (LCM) is a new antiepileptic drug used as an adjunctive treatment for partial seizures with and without secondary generalization. One of the modes of action is the enhancement of slow inactivation of voltage-gated sodium channels. Experimental studies and clinical trials suggest that LCM acts upon both neurons and the heart and may increase the risk of cardiac arrhythmias. A systematic review was conducted to investigate characteristics of arrhythmias related to the use of LCM for the treatment of seizures. The search terms “lacosamide”, “arrhythmias”, “AV block”, “atrial fibrillations/flutter”, “cardiac conductions defects”, “ventricular tachycardia”, “ventricular fibrillation were used. Case reports and retrospective studies were gathered by searching Medline/PubMed, Google Scholar, CINAHL (Cumulative Index to Nursing and Allied Health Literature), Cochrane CENTRAL (Cochrane Central Register of Controlled Trials), and Web of Science databases. Seventeen articles were selected for review. Ventricular tachycardia was the most reported LCM related arrhythmia (29.4%), followed by new-onset atrial fibrillation (17.6%), complete heart block (17.6%), Mobitz type 1 Atrio-ventricular block (11.8%), sinus pauses (11.8%), pulseless electrical activity (5.9%) and widening QRS complex (5.9%). Further research and clinical trials are needed to explore the etiopathogenesis and causative relationship between the use of LCM and arrhythmias.
Vascular Closure Devices (VCD) are routinely used in cardiac catheterization and other endovascular procedures in order to achieve immediate post-procedural hemostasis and sealing of the femoral artery puncture site. Unlike manual compression, VCD encompass a broad range of devices, with varying mechanisms, that offer the advantage of achieving rapid hemostasis, increased patient comfort and mobility, decreased reliance on hospital staff resources, and facilitate earlier hospital discharge. Complications of VCD have been well-described and include embolization, arterial occlusion, infection, or vascular obstruction. Here, we describe a case in which the Angio-Seal device was utilized during an elective cardiac catheterization resulted in acute lower extremity ischemia.
Coronavirus disease 2019 , caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was first identified in Wuhan, China in December 2019. Since then, the disease has spread globally, leading to the ongoing pandemic. It can cause severe respiratory illness; however, many cases of pericarditis have also been reported. This systematic review aims to recognize the clinical features of pericarditis and myopericarditis in COVID-19 patients.Google Scholar, Medline/PubMed, CINAHL, Cochrane Central, and Web of Science databases were searched for studies reporting "Coronavirus" or "COVID" and "Peri-myocarditis," "heart," or "retrospective." Case reports and retrospective studies published from May 2020 to February 2021 were reviewed.In total, 33 studies on pericarditis, myopericarditis, and pericardial infusion were included in this review. COVID-19 pericarditis affected adult patients at any age. The incidence is more common in males, with a male-to-female ratio of 2:1. Chest pain (60%), fever (51%), and shortness of breath (51%) were the most reported symptoms, followed by cough (39%), fatigue (15%), myalgia (12%), and diarrhea (12%). Laboratory tests revealed leukocytosis with neutrophil predominance, elevated D-dimer, erythrocyte rate, and Creactive protein. Cardiac markers including troponin-1, troponin-T, and brain natriuretic peptide were elevated in most cases. Radiographic imaging of the chest were mostly normal, and only 31% of chest X-rays showed cardiomegaly and or bilateral infiltration. Electrocardiography (ECG) demonstrated normal sinus rhythm with around 59% ST elevation and rarely PR depression or T wave inversion, while the predominant echocardiographic feature was pericardial effusion. Management with colchicine was favored in most cases, followed by non-steroidal anti-inflammatory drugs (NSAIDs), and interventional therapy was only needed when patient developed cardiac tamponade. The majority of the reviewed studies reported either recovery or no continued clinical deterioration.The prevalence of COVID-19-related cardiac diseases is high, and pericarditis is a known extrapulmonary manifestation. However, pericardial effusion and cardiac tamponade are less prevalent and may require urgent intervention to prevent mortality. Pericarditis should be considered in patients with chest pain, ST elevation on ECG, a normal coronary angiogram, and COVID-19. We emphasize the importance of clinical examination, ECG, and echocardiogram for decision-making, and NSAIDs, colchicine, and corticosteroids are considered to be safe in the treatment of pericarditis/myopericarditis associated with COVID-19.
Spontaneous coronary artery dissection (SCAD) is a cardiac emergency and an uncommon cause of acute coronary syndrome (ACS) with a higher predominance in younger women. It is a non-traumatic, non-atherosclerotic lesion found to be associated with pregnancy, inflammatory disorders, connective tissue diseases and substance abuse. Our patient was a young woman with a chronic marijuana smoking history who was found to have a NSTEMI. Initial angiogram showed triple vessel disease involving left anterior descending artery (LAD), left circumflex artery (LCX) and obtuse marginal artery (OM). A repeat angiogram notably showed spontaneous progression with dissection in all three vessels attributable to substance abuse. We present you this rare occurrence of triple vessel SCAD secondary to marijuana with a literature review and discussion.
Background. Myasthenic crisis can induce Takotsubo cardiomyopathy leading to transient systolic and diastolic left ventricular dysfunction and wall-motion abnormalities, including the characteristic apical ballooning. We aimed to define the clinical features of this disease entity. Methods. A systematic review was conducted to examine the characteristics of Takotsubo cardiomyopathy presenting in myasthenia gravis patients. Case reports were accessed by searching MEDLINE/PubMed, Google Scholar, CINAHL, and Web of Science databases. 523 articles were identified and 14 were selected for review. Results. Takotsubo cardiomyopathy presenting in myasthenia gravis' patients tends to affect women between the ages of 40 to 77. History of atrial fibrillation or hypertension was found in a minority of cases. Generalized weakness, fatigue, dysphagia and respiratory distress were common at presentation. Vital signs demonstrated normal blood pressure without tachycardia or bradycardia. Elevated values of troponins, creatine kinase (CK), and CK-MB isoenzymes were recorded. ST-segment elevation followed by T-wave inversion were predominantly found on electrocardiograms. Apical abnormalities in the form of ballooning, hypokinesia, or sparing and reduced left ventricular ejection fraction (≤45%) were observed using transthoracic echocardiogram or left ventriculography. Coronary angiography demonstrated no obstructive lesions. Ventilatory support, cholinesterase inhibitors and glucocorticoids resulted in the recovery or improvement of the left ventricular ejection fraction and hemodynamic stability. Only a minority of patients died of refractory heart failure. Treatment with inotropes and/or vasopressors led to poorer outcomes, including death or intractable heart failure. Conclusion. The management of Takotsubo cardiomyopathy developing in myasthenia gravis patients should focus on addressing the myasthenic crisis, while proving supportive care in and intensive care setting.
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