Chronic congestive heart failure (CHF) is a complex disorder characterized by inability of the heart to keep up the demands on it, followed by the progressive pump failure and fluid accumulation. Although the loop diuretics are widely used in heart failure (HF) patients, both pharmacodynamic and pharmacokinetic alterations are thought to be responsible for diuretic resistance in these patients. Strategies to overcome diuretic resistance include sodium intake restriction, changes in diuretic dose and route of administration and sequential nephron diuretic therapy. In this review, we discuss the definition, prevalence, mechanism of development and management strategies of diuretic resistance in HF patients.

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Heart failure (HF) is recognized as one of the leading causes of morbidity and mortality worldwide. Every year about 500,000 new cases of HF are diagnosed in the United States. The predominant etiology of death in HF patients include sudden cardiac death (SCD) and pump failure. Prediction of mode of death may help in devising management decisions. In patients with HF, the presence of myocardial fibrosis has been a known risk factor for SCD and thus it could be used as a criterion in risk stratification for SCD. However, the underlying pathophysiology of SCD is uncertain and controversial, which makes it necessary to develop newer tools to enhance SCD risk stratification. The newer tools should be innovative enough either to complement or to replace the currently available tools. In this scoping review, we highlighted the utilization of novel biomarkers galectin-3 (gal-3) and soluble ST2 (sST2) and discussed that how they might complement currently available tools such as, cardiac MRI (CMR) for SCD risk stratification in HF patients.

Congenital coronary artery anomalies are rare disease entities, occur only in 0.3%−5.6% of the general population. These anomalies could lead to serious complications in some cases and is associated with associated with sudden death due to lethal arrhythmias and premature coronary artery disease. Diagnosis of these anomalies is generally made during angiography. In this report, we present a rare case of absent left main coronary artery and anomalous origins of left anterior descending artery and left circumflex artery from right sinus of Valsalva in a 62 year old man presented with non-ST elevation myocardial infarction (NSTEMI).

We present a case of simultaneous cardiotoxicity and stroke-like neurotoxicity in a patient treated with FOLFOX, a 5-Fluorouracil (5-FU)-containing chemotherapy regimen. Within hours of FOLFOX infusion, the patient began to exhibit signs and symptoms of myocardial ischemia and stroke mimic. Coronary vasoconstriction and vasospasm is a known mechanism of 5-FU-induced cardiotoxicity. 5-FU-induced neurotoxicity commonly presents as encephalopathy and is likely attributable to the accumulation of ammonia, a product of 5-FU metabolism. However, our patient presented with focal neurological signs and normal levels of ammonia. This suggests that 5-FU-induced vasospasm in the coronary arteries and cerebral vasculature is a likely cause of the simultaneous cardiac and neurological events we report here which have not been reported previously. Recognition of these toxicities as complications of 5-FU chemotherapy is crucial for the proper diagnosis and treatment of patients.