BackgroundMany Muslim type 2 diabetes mellitus (T2DM) patients choose to fast the month of Ramadan despite the possible adverse health effects brought about by the change in dietary habits, among other things. Clinical data regarding the safety of multi-drug regimens during fasting are particularly scarce. The aim of the study was to evaluate the safety of a drug protocol devised by the authors to accommodate Ramadan's dietary changes, involving dose adjustments of four anti-diabetic drug regimens in T2DM patients fasting Ramadan.MethodsIn this prospective, observational, open-label study, 301 T2DM patients who wished to fast Ramadan were followed during Ramadan and the preceding month. The incidence of hypoglycemia, diabetic ketoacidosis (DKA) and non-ketotic hyperosmolar state (NKHS) was monitored. Patients were classified into four groups: A group (those taking metformin, sulfonylurea and insulin [n=33]); B group (metformin and sulfonylurea [n=89]); C group (metformin and insulin [n=96]); and D group (premixed 70/30, glargine or regular insulin [n=82]). During Ramadan, drug doses were adjusted as percentages of their pre-Ramadan values: 75% for sulfonylureas, 75% for glargine, 75% for premixed insulin 70/30 in two doses, and 75% for regular insulin. Metformin was adjusted to a twice-daily regimen.ResultsNo cases of DKA or NKHS were reported. Hypoglycemia occurred at a lower rate than pre-Ramadan values in groups C, and D; and a similar rate in groups A, and B.ConclusionThe data suggested that using the above protocol to adjust the doses of anti-diabetic drugs is safe in T2DM patients in regards to hypoglycemia, DKA, and NKHS.
Evidence linking cocaine to the risk of pulmonary hypertension (PH) is limited and inconsistent. We examined whether cocaine use, in the absence of other known causes of PH, was associated with elevated systolic pulmonary artery pressure (sPAP) and increased probability of PH. We compared patients with documented cocaine use to a randomly selected age, sex, and racematched control group without history of cocaine use. All participants had no known causes of PH and underwent echocardiography for noninvasive estimation of sPAP. We used routinely reported echocardiographic parameters and contemporary guidelines to grade the probability of PH. In 88 patients with documented cocaine use (mean age ± standard deviation 51.7 ± 9.5 years), 33% were women and 89% were of Black race. The commonest route of cocaine use was smoking (74%). Cocaine users compared with the control group had significantly higher sPAP (mean ± standard deviation, 30.1 ± 13.1 vs 22.0 ± 9.8 mm Hg, p <0.001) and greater likelihood of PH (25% vs 10%, p = 0.012). In multivariable analyses adjusted for potential confounders including left ventricular diastolic dysfunction, cocaine use conferred a fivefold greater odds of echocardiographic PH (p = 0.006). Additionally, a stepwise increase in the likelihood of PH was noted across cocaine users with negative or no drug screen on the day of echocardiography to cocaine users with a positive drug screen (multivariable p for trend = 0.008). In conclusion, cocaine use was associated with a higher sPAP and an increased likelihood of echocardiographic PH with a probable acute-onchronic effect.
Thrombotic thrombocytopenic purpura (TTP) is a multisystem disease characterized by disseminated thrombus formation in the arterioles and capillaries. Patients usually present with weakness, subtle mental changes, fever, and acute kidney injury. Cardiac symptoms, such as chest pain or arrhythmia, have been reported but were rarely the sole presenting symptom. We report the case of a 68-year-old woman with acute non-ST-elevation myocardial infarction who was found to have TTP. Prompt diagnosis of TTP is essential because traditional approaches to manage an acute coronary event, inclusive of dual antiplatelet therapy and percutaneous coronary intervention, might be contraindicated due to an increased risk of bleeding. Early administration of steroids and urgent initiation of plasmapheresis to improve platelet count would be crucial initial steps in the management of these patients.
BACKGROUND The effects of carvedilol and metoprolol succinate on appropriate and inappropriate implantable cardioverter defibrillator (ICD) therapy in patients with heart failure with reduced ejection fraction (HFrEF) are not fully understood. HYPOTHESIS The hypothesis of our study is possible carvedilol superiority over metoprolol in patients with ICD. METHODS All patients with ICD registered to a single device clinic between 1/2012 and 6/2017 (n = 569) were identified. Patients with systolic heart failure (left ventricular ejection fraction ≤40%) treated with carvedilol vs metoprolol succinate were compared. Primary endpoint was difference in survival free of appropriate device therapy (shock or anti‐tachycardia pacing, ATP). Secondary endpoints were freedom from inappropriate therapy (shock or ATP) and all cause death. RESULTS A total of 225 patients were included in the analysis with median follow up of 57 months (IQR 33.7‐90). The 2 groups were comparable in the baseline characteristics. Carvedilol was superior to metoprolol succinate in improving survival free of appropriate ICD therapy (HR 0.42; 95% CI 0.24‐0.72, P = 0.01). This difference was driven by reduction in survival free of appropriate shocks (HR 0.30; 95% CI 0.15‐0.63, P = −0.01) while there was no significant difference in appropriate ATP (HR 0.55; 95% CI 0.28‐1.1, P = 0.12). There was no significant difference in time to inappropriate shocks (HR 1.02; 95% CI 0.19‐5.6, P = 0.97), inappropriate ATP (HR 0.93, OR 0.24‐3.5, p value 0.9) or all cause death (HR 0.8; 95% CI 0.42‐1.5, P = 0.52). CONCLUSIONS This study suggests that carvedilol use was associated with improved survival free of appropriate ICD therapy compared to metoprolol succinate in patients with HFrEF.
The measurement of cardiac troponin, released from injured cardiomyocytes, is of paramount importance in the diagnosis of acute myocardial infarction. Elevated troponin can be encountered, however, in patients with cardiomyopathy, significant cardiac arrhythmias, vasculitis, right-sided heart strain, critical systemic illnesses, stroke, drug toxicity (such as Adriamycin), poisons (such as snake venoms), renal failure, seizure, and rhabdomyolysis. If the clinical picture is not consistent with any of these causes, a false-positive result should be considered. We herein describe a 94-year-old man with a prior history of coronary artery disease who presented with altered mental status and was found to have a persistently high troponin level resulting in three admissions to the coronary care unit for various noncardiac complaints. Because of discordance between clinical and laboratory data, immunological interference due to heterophile antibodies in the locally used assay (AccuTnI+3, Beckman Coulter) was suspected. The same serum sample tested on a different assay (Elecsys Troponin I Assay, Roche) resulted in an undetectable cardiac troponin I level, thus confirming the diagnosis.
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