Chorea gravidarum treated with chlorpromazine; case report.

American Journal of Obstetrics and Gynecology

Chronic kidney disease (CKD) is the most common cause of end-stage renal disease in patients with type 2 diabetes mellitus (T2DM). CKD increases the risk of cardiovascular diseases; therefore, its prevention and treatment are important. The prevention of diabetic kidney disease (DKD) can be achieved through intensive glycemic control and blood pressure management. Additionally, DKD treatment aims to reduce albuminuria and improve kidney function. In patients with T2DM, renin-angiotensin-aldosterone system inhibitors, sodium glucose cotransporter 2 inhibitors, and glucagon-like peptide-1 receptor agonists can delay the progression of DKD. Hence, there is a need for novel treatments that can effectively suppress DKD progression. Finerenone is a first-in-class nonsteroidal mineralocorticoid receptor antagonist with clinically proven efficacy in improving albuminuria, estimated glomerular filtration rate, and risk of cardiovascular events in early and advanced DKD. Therefore, finerenone is a promising treatment option to delay DKD progression. This article reviews the mechanism of renal effects and major clinical outcomes of finerenone in DKD.

Renal Protection of Mineralocorticoid Receptor Antagonist, Finerenone, in Diabetic Kidney Disease.

Endocrinology and Metabolism

Cardiomyopathies are a heterogeneous group of structural, mechanical, and electrical heart muscle disorders which often correlate with life-threatening arrhythmias and progressive heart failure accounting for significant cardiovascular morbidity and mortality. Currently, cardiomyopathies still represent a leading reason for heart transplantation worldwide. The last years have brought remarkable advances in the field of cardiomyopathies especially in terms of understanding the molecular basis as well as the diagnostic evaluation and management. Although most cardiomyopathy treatments had long focused on symptom management, much of the current research efforts aim to identify and act on the disease-driving mechanisms. Regarding risk assessment and primary prevention of sudden cardiac death, additional data are still pending in order to pave the way for a more refined and early patient selection for defibrillator implantation. This review summarizes the current knowledge of hypertrophic, dilated and arrhythmogenic cardiomyopathy with a particular emphasis on their pathophysiology, clinical features, and diagnostic approach. Furthermore, the relevant ongoing studies investigating novel management approaches and main gaps in knowledge are highlighted.

Hypertrophic, Dilated, and Arrhythmogenic Cardiomyopathy: Where Are We?

Biomedicines

Background Ventricular ectopy is observed in most of the population ranging from isolated premature ventricular contractions to rapid hemodynamically unstable ventricular tachyarrhythmias like ventricular tachycardia and ventricular fibrillation. Multiple mechanisms exist for ventricular arrhythmias such as triggered activity, reentry, and automaticity. Scar-based reentry forms the basis of most malignant VA that can lead to sudden cardiac death. Many antiarrhythmic drugs have been utilized for the suppression of ventricular arrhythmia. They are commonly classified using the Vaughan-Williams-Singh classification which distinguishes them based on the predominant action on different phases of the cardiac action potential. Class Ic agents are widely used in premature ventricular contraction suppression but are contraindicated in patients with prior myocardial infarction or ischemic scar, and heart failure. Beta-blockers continue to be a mainstay in the treatment of most symptomatic VA and are well tolerated, relatively safe, and have additional benefits in symptomatic coronary heart disease and left ventricular systolic dysfunction. Amiodarone continues to be used for the management of most cases of serious VA especially in the acute setting when accompanied by hemodynamic perturbations but has the disadvantage of having a poor toxicity profile for long-term use Summary Historically used for long-term ventricular arrhythmia suppression and prevention of sudden cardiac death, antiarrhythmics are now used to reduce implantable defibrillator shocks and symptoms. They still have a role in premature ventricular complex suppression in patients with failed catheter ablation or those who are not candidates for invasive therapy. Newer concepts in cardiac imaging and the use of artificial intelligence may help further delineate sudden cardiac risk and identify patients that may benefit from pharmacological management. Key Message Anti-arrhythmic agents continue to perform an important role in the suppression of ventricular arrhythmias especially channelopathies, polymorphic VT, and idiopathic ventricular fibrillation. Judicious use of these agents while recognizing side effects can help reduce the long-term effects of ventricular arrhythmias on cardiac function.

Pharmacotherapy in Ventricular Arrhythmias.

Cardiology

Sepsis-associated acute kidney injury (SA-AKI) is common in critically ill patients and is strongly associated with adverse outcomes, including an increased risk of chronic kidney disease, cardiovascular events and death. The pathophysiology of SA-AKI remains elusive, although microcirculatory dysfunction, cellular metabolic reprogramming and dysregulated inflammatory responses have been implicated in preclinical studies. SA-AKI is best defined as the occurrence of AKI within 7 days of sepsis onset (diagnosed according to Kidney Disease Improving Global Outcome criteria and Sepsis 3 criteria, respectively). Improving outcomes in SA-AKI is challenging, as patients can present with either clinical or subclinical AKI. Early identification of patients at risk of AKI, or at risk of progressing to severe and/or persistent AKI, is crucial to the timely initiation of adequate supportive measures, including limiting further insults to the kidney. Accordingly, the discovery of biomarkers associated with AKI that can aid in early diagnosis is an area of intensive investigation. Additionally, high-quality evidence on best-practice care of patients with AKI, sepsis and SA-AKI has continued to accrue. Although specific therapeutic options are limited, several clinical trials have evaluated the use of care bundles and extracorporeal techniques as potential therapeutic approaches. Here we provide graded recommendations for managing SA-AKI and highlight priorities for future research.

Sepsis-associated acute kidney injury: consensus report of the 28th Acute Disease Quality Initiative workgroup.

Nature Reviews. Nephrology

The current review is to describe the definition and prevalence of resistant arterial hypertension (RAH), the difference between refractory hypertension, patient characteristics and major risk factors for RAH, how RAH is diagnosed, prognosis and outcomes for patients.

According to the WHO, approximately 1.28 billion adults aged 30-79 worldwide have arterial hypertension, and over 80% of them do not have blood pressure (BP) under control. RAH is defined as above-goal elevated BP despite the concurrent use of 3 or more classes of antihypertensive drugs, commonly including a long-acting calcium channel blocker, an inhibitor of the renin-angiotensin system (angiotensin-converting enzyme inhibitor or angiotensin receptor blocker), and a thiazide diuretic administered at maximum or maximally tolerated doses and at appropriate dosing frequency. RAH occurs in nearly 1 of 6 hypertensive patients. It often remains unrecognised mainly because patients are not prescribed &#x2265;3 drugs at maximal doses despite uncontrolled BP.

RAH distinctly increases the risk of developing coronary artery disease, heart failure, stroke and chronic kidney disease and confers higher rates of major adverse cardiovascular events as well as increased all-cause mortality. Timely diagnosis and treatment of RAH may mitigate the associated risks and improve short and long-term prognosis.

Chorea gravidarum treated with chlorpromazine; case report.

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Chorea gravidarum treated with chlorpromazine; case report.

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