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Coronary no-reflow phenomenon is a lethal mechanism of ongoing myocardial injury, following successful revascularization of an infarct-related coronary artery. Incidence of this phenomenon is high following percutaneous intervention, and is associated with adverse in-hospital and long-term outcomes. Several mechanisms such as ischemia-reperfusion injury and distal microthromboembolism in genetically susceptible patients and those with preexisting endothelial dysfunction have been implicated. However, the exact mechanism in humans is still poorly understood. Several investigative and treatment strategies within and outside the cardiac catheterization laboratory have been proposed, but have not uniformly shown success in reducing mortality or in preventing adverse left ventricular remodeling resulting from this condition. The aim of this article is to provide a brief and concise review of the current understanding of the pathophysiology, clinical predictors, and investigations and management of coronary no-reflow phenomenon.

Sepsis is a clinical syndrome with physiologic and biochemical derangements caused by dysregulated inflammatory response to an infection. A recent retrospective study showed that vitamin C, hydrocortisone and thiamine in intensive care unit (ICU) patients with septic shock when added to standard care improved mortality and outcomes. We undertook a prospective single-blinded study to evaluate effects of addition of this triple therapy to standard ICU care on 28-day mortality in patients with septic shock. METHODS: Patients at LAC+USC Medical Center with septic shock defined as sepsis-induced hypotension requiring vasopressors with serum lactate level >2 mmol/L were enrolled within 24 hours of identification. Exclusion criteria included inability to obtain consent, incarceration, active malignancy, dementia, pregnancy or lactation, active ischemic or hemorrhagic stroke, active cardiogenic or other causes of shock, history of renal stones and current use of steroids. Patients were blinded as to treatment group and randomized by a blinded operator in block randomization in a 1:1 fashion in groups of 8. Patients received either standard ICU care (control) or standard care plus intravenous (IV) Vitamin C 1.5 gram every 6 hours for 4 days or until ICU discharge, IV hydrocortisone 50 mg every 6 hours for 7 days or until ICU discharge, and IV thiamine 200 mg every 12 hours for 4 days or until ICU discharge. Data were analyzed using SPSS with a chi squared test. P-value <0.05 was considered statistically significant.

Coronary no-reflow phenomenon is a lethal mechanism of ongoing myocardial injury following successful revascularization of an infarct-related coronary artery. Incidence of this phenomenon is high following percutaneous intervention and is associated with adverse in-hospital and long-term outcomes. Several mechanisms such as ischemia-reperfusion injury and distal microthromboembolism in genetically susceptible patients and those with preexisting endothelial dysfunction have been implicated. However, the exact mechanism in humans is still poorly understood. Several investigative and treatment strategies within and outside the cardiac catheterization laboratory have been proposed, but they have not uniformly shown success in reducing mortality or in preventing adverse left ventricular remodeling resulting from this condition. The aim of this article is to provide a brief and concise review of the current understanding of the pathophysiology, clinical predictors, and investigations and management of coronary no-reflow phenomenon.

Myocardial infarction with nonobstructive coronary arteries (MINOCA) is a complex clinical syndrome that is characterized by evidence of acute myocardial infarction in the absence of significant epicardial coronary artery disease on angiography. The term “MINOCA” encompasses a group of heterogeneous diseases with varying underlying mechanisms and each with its own pathophysiology. Overlooked plaque rupture or erosion and coronary vasospasm are the most common causes of MINOCA and can be diagnosed by routine intracoronary imaging and vasoreactivity testing, respectively. Coronary microvascular dysfunction is a less recognized, albeit an important cause of morbidity in patients presenting with MINOCA. Although MINOCA is a rare presentation of acute coronary syndrome, it is not a benign disorder and can have adverse consequences if untreated. In this article, we aim to review the pathogenesis, clinical characteristics, and finally propose a systematic approach in the diagnosis and management of patients with MINOCA.

Objective: Sickle cell disease (SCD) is a multifaceted, chronic disease severely affecting the quality of life of patients and their families. In addition, it is becoming a costly public health concern. In comparing the epidemiology, management and outcome of SCD in the United States of America and the Caribbean, this article aimed to promote awareness of SCD and the need for adequate treatment. Methods: The surveillance data for SCD patients in Grenada were collected from the General Hospital of Grenada (St George's, Grenada) from discharge sheets that were filled out with the diagnosis of the patient and the cause of death. The data included the number of patients with SCD admitted to the hospital from 2007 to 2013, along with the number of individuals with SCD who died during each year. Results: Based on the given data, the average prevalence of SCD was approximately 1.49 per 1000 persons per year. The average case-fatality rate was 1.10%, and the average causespecific mortality rate was 1.64 per 100 000 persons per year. Conclusion: The lack of continuous registered follow-up of patients with SCD and the lack of preventive care, especially in developing countries, still results in the early deaths of patients. The data validated the severity of SCD in Grenada, and were compared with the data available in Haiti and Jamaica, in order to stress the importance of implementing better follow-up care to decrease the incidence and mortality of this devastating disease. Proper data collection and guidelines for basic care are needed to improve the quality of life of the patients with SCD in Grenada and the rest of the Caribbean region.

A miliary pattern depicting a diffuse micronodular lung disease was previously seen as a pathognomonic for the lymphohematogenous spread of Mycobacterium tuberculosis. We present a case of vaping-associated lung injury with a novel pattern of diffuse, ill-defined centrilobular miliary micronodules with a tree-in-bud distribution, related to the development of small airway disease. CASE PRESENTATION: A 55-year-old male with a history of asthma presented with shortness of breath and cough for 1 month. He endorsed excessive vaping-use of about 100 mL of flavored nicotine per week utilizing a tank device. He was tachypneic and hypoxemic, with neutrophil-predominant leukocytosis and elevated CRP 152. Chest CT showed diffusely-distributed, ill-defined centrilobular micronodular opacifications (<4mm) with a tree-in-bud pattern, subpleural sparing, and interlobular septal thickening. Infectious disease work-up was negative, aside from one positive sputum culture of Mycobacterium Chlelonae Complex. On day 10, a transbronchial biopsy was performed, which was complicated by severe bronchospasms, bleeding and hypercapnic respiratory failure requiring prolonged intubation. Biopsy showed focal interstitial inflammation and patchy nonspecific pneumonitis, with no airway fragments for investigation. He was empirically treated with broad-septum antibiotics, RIPE therapy, and Ambisome without significant improvement. The patient was then started on corticosteroid therapy. A repeat CT showed a mild decrease in the micronodular opacities, and a concern for the development of early bronchiectasis. On day 35, the patient was discharged.

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