Exploring Disparities in Mortality Rates Among Heart Failure Patients With Primary Diagnosis of Cardiac Arrest: A Nationwide Analysis of 2016-2020 Data.

Cardiac arrest is a dangerous threat to patients with heart failure. In this analysis, the authors aim to investigate the disparities between patients with heart failure who died with a diagnosis of cardiac arrest in terms of race, income, sex, hospital location, hospital size, hospital region, and insurance. Do social determinants of life impact cardiac arrest in patients with heart failure? A total of 8840 patients with heart failure who had a primary diagnosis of cardiac arrest, were admitted non-elective, were adults, and died during the admission were included in this study. A total of 215 (2.43%) patients had cardiac arrest due to cardiac cause, 95 (1.07%) had cardiac arrest due to other specified causes, and 8530 (96.49%) patients had cardiac arrest due to unspecified cause. The study group had a mean age of 69 years and had more males (53.91%). In terms of cardiac arrest due to any cause among adult patients with heart failure, the difference was significantly different in female patients (OR 0.83, p-value = 0.001, 95% CI 0.74-0.93), Black patients (OR 1.44, p-value < 0.001, 95% CI 1.25-1.67), Asian patients (OR 1.66, p-value = 0.002, 95% CI 1.20-2.29), Native American patients (OR 1.96, p-value = 0.022, 95% CI 1.10-3.48), other race patients (OR 1.59, p-value = 0.007, 95% CI 1.14-2.23), patients on hospital from south region (OR 1.59, p-value = 0.007, 95% CI 1.14-2.23), patients from large hospitals (OR 1.21, p-value = 0.015, 95% CI 1.04-1.41), and patients from teaching hospitals (OR1.19, p-value = 0.018, 95% CI 1.03-1.37). In terms of cardiac arrest due to cardiac cause among adult patients with heart failure, there was no significant difference in the variables analyzed. In terms of cardiac arrest due to other specified causes among adult patients with heart failure, the difference was significantly different in female patients (OR 0.19, p-value = 0.024, 95% CI 0.04-0.80), and urban-based hospitals (OR 0.10, p-value = 0.015, 95% CI 0.02-0.64). In terms of cardiac arrest due to unspecified causes among adult patients with heart failure, the difference was significantly different in female patients (OR 0.84, p-value = 0.004, 95% CI 0.75-0.95), Black patients (OR 1.46, p-value < 0.001, 95% CI 1.26-1.69), Asian patients (OR 1.60, p-value = 0.006, 95% CI 1.14-2.23), Native American patients (OR 2.06, p-value = 0.014, 95% CI 1.16-3.67), other race patients (OR 1.58, p-value = 0.010, 95% CI 1.12-2.23), patients on the hospital from the south region (OR 1.25, p-value = 0.014, 95% CI 1.05- 1.48), patients on the hospital from Midwest region (OR 1.22, p-value = 0.033, 95% CI 1.02-1.46), patients from large hospitals (OR 1.21, p-value = 0.016, 95% CI 1.04-1.41), patients from teaching hospitals (OR 1.18, p-value = 0.022, 95% CI 1.02-1.36), patients from urban hospitals (OR 1.37, p-value = 0.023, 95% CI 1.04-1.80). In conclusion, it is imperative for physicians to remain cognizant of health disparities while assessing patients to preempt bias during the evaluation process. The present analysis convincingly demonstrates the influence of gender, race, and hospital location on the incidence of cardiac arrest in individuals afflicted with heart failure. Nonetheless, the paucity of cases pertaining to cardiac arrest attributed to cardiac causes or other specified etiologies considerably compromises the analytical robustness for this particular subtype of cardiac arrest. Thus, further investigations are warranted to ascertain the underlying factors contributing to such disparities among patients with heart failure, while concurrently necessitating physicians' awareness regarding the potential existence of bias in their evaluative endeavors.

Management of hypertension in liver transplant patients.

Hypertension is a common co-morbidity and a frequent complication in liver transplant patients. The aim of this paper is to concisely review available clinical data and propose a hypertension treatment algorithm in liver transplant patients. Calcium channel blockers are mainstay of the treatment due to their potent vasodilatory effects. Dihydropyridine calcium channel blockers are preferable due to their least interaction with cytochrome P450 enzyme system and, therefore, minimal risk of potential disruption of immunosuppressive drug levels. Beta-blockers may be considered first line drugs in patients with resting tachycardia and in those with high cardiac outputs. Data support the use of beta-blockers for patients intolerant or unresponsive to calcium channel blockers. Angiotensin converting enzyme inhibitors and angiotensin receptor blockers have little value when used early after liver transplant but may have a more pronounced role during the later periods. Diuretics may be of value in combination with other drugs, especially to counteract the potassium-retaining effects of calcineurin inhibitors. Treatment of post liver transplantation hypertension in patients with co-morbid conditions such as coronary artery disease, diabetes mellitus, congestive heart failure, and renal disease will likely require combination therapy.

Isolated noncompaction cardiomyopathy presenting with paroxysmal supraventricular tachycardia--case report and literature review.

Isolated noncompaction cardiomyopathy is an exceedingly rare congenital cardiomyopathy. A case of isolated noncompaction cardiomyopathy is reported and the literature on the subject collected through a comprehensive literature search is reviewed. Fewer than 100 cases of this condition have been reported. Isolated noncompaction cardiomyopathy is caused by a defect in cardiac morphogenesis resulting in an arrest of compaction of loose interwoven meshwork of myocardial fibers during intrauterine life, which results in severe systolic dysfunction as well as undue hypertrophy of the involved walls of the ventricles. Although the most frequent sites involved are left ventricular apex and inferior wall, involvement of other left ventricular walls and right ventricle has also been reported. Etiology of the isolated noncompaction of myocardium is not clear. Familial cases have been reported and the mode of inheritance is heterogeneous. In X-linked form of the disease, a locus has been found on Xq28, and mutations have been reported in G4.5 gene. The age of onset of symptoms ranges from infancy to the geriatric age. Patients with isolated noncompaction cardiomyopathy have a high incidence of heart failure, arrhythmias, and thromboembolism. The most common presentation is congestive heart failure. Arrhythmias include atrial arrhythmias, ventricular tachycardia, and sudden cardiac death. The patient reported in this article presented with paroxysmal supraventricular tachycardia. Echocardiography is the procedure of choice to establish diagnosis. Due to the lack of associated cardiac anomalies, antenatal detection is difficult. The treatment is that for congestive heart failure, arrhythmias, and thromboembolism. The end-stage congestive heart failure is managed with heart transplantation and potential life-threatening ventricular tachyarrhythmias with an implantable cardioverter defibrillator. Prognosis is poor and the common causes of death are intractable heart failure and sudden cardiac death.

Differential effect of glyburide (glibenclamide) and metformin on QT dispersion: a potential adenosine triphosphate sensitive K+ channel effect.

Glyburide (glibenclamide) is a specific blocker of the adenosine triphosphate (ATP) sensitive potassium (K+) channel. It has been reported to result in prolongation of the QT interval. QT interval dispersion (QTd) is a potentially sensitive marker for increased risk of arrhythmia and sudden cardiac death. The aim of the present study was to evaluate the effect of glyburide on QTd and compare it with that of metformin, a hypoglycemic agent that does not block the adenosine triphosphate sensitive K+ channel. Thirty patients with type 2 diabetes were randomized to glyburide and metformin groups. A 12-lead electrocardiogram was obtained before and at 2 months after being on glyburide or metformin. Therapy with QT and QTd were measured and QT corrected for rate (QTc). There was no significant difference between the glyburide and metformin groups in age (62 +/- 9 vs 59 +/- 10 years), baseline RR interval (819 +/- 86 vs 753 +/- 100 ms), QT (387 +/- 28 vs 383 +/- 27 ms), and QTc (433 +/- 25 vs 444 +/- 15 ms). Glyburide was associated with a significant increase in QTc (433 +/- 24 to 467 +/- 24 ms, p <0.001), QTd (24 +/- 16 to 60 +/- 22 ms, p <0.001), and QTc dispersion (QTcd) (35 +/- 18 to 68 +/- 21 ms, p <0.001). In contrast, metformin was associated with a decrease in QTc (444 +/- 15 to 432 +/- 15 ms, p <0.01) and did not affect QTd (14 +/- 5 to 12 +/- 6 ms, p = NS) and QTcd (23 +/- 9 to 22 +/- 10 ms, p = NS). Glyburide, unlike metformin, causes an increase in QT dispersion. Increased dispersion may be a factor underlying an increased risk of arrhythmias and sudden cardiac death.