Myogenic Underactive Bladder and Heart Failure Resemblance: A Novel Role for SGLT2 Inhibition?

Gabriel Faria-Costa1, Ana Charrua2, Carlos Martins-Silva3

  • 1Department of Urology, Local Health Unit of Matosinhos, Matosinhos, Portugal; Department of Surgery and Physiology, Faculty of Medicine, University of Porto, Porto, Portugal; Cardiovascular Research and Development Center, Faculty of Medicine, University of Porto, Porto, Portugal.

Insights

Heart failure and myogenic underactive bladder share similar muscle injury pathways. SGLT2 inhibitors, effective for heart failure, may offer a new treatment for myogenic underactive bladder.

Area of Science:

  • Urology
  • Cardiology
  • Pharmacology

Background:

  • Heart failure (HF) and myogenic underactive bladder (mUAB) exhibit comparable pathophysiology, including muscle injury linked to disease severity.
  • Both conditions progress to advanced stages characterized by myocardial and detrusor fibrosis, resulting in reduced contractility.

Purpose of the Study:

  • To explore the pathophysiological similarities between HF and mUAB.
  • To investigate the potential therapeutic role of SGLT2 inhibitors in treating mUAB, drawing parallels with their efficacy in HF.

Main Methods:

  • This mini-review synthesizes existing literature on the biomechanics and pathophysiology of HF and mUAB.
  • It examines the shared mechanisms of muscle injury and fibrosis in both conditions.
  • It evaluates the established pharmacological treatments for HF and considers their potential applicability to mUAB.

Main Results:

  • HF and mUAB share commonalities in muscle injury and fibrosis, impacting contractility in both the heart and bladder.
  • Currently, effective pharmacological treatments for mUAB are lacking, unlike established therapies for HF.

Conclusions:

  • The shared pathophysiological pathways between HF and mUAB suggest a potential therapeutic avenue.
  • SGLT2 inhibitors, demonstrating success in HF treatment, are hypothesized to be beneficial for mUAB, offering a novel treatment strategy.

Related Concept Videos

Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
69
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
507
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
529
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
754
Heart Failure V: Medical Management01:30

Heart Failure V: Medical Management

Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...
36
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
1.9K