Apical Hypokinesis in a Patient with Hypertrophic Cardiomyopathy and Myocardial Bridging: Reversal with Beta-Blockade

Rentoukas, Elias; Deftereos, Spyros; Alpert, Martin A.; Nikas, Dimitris J.; Lazaros, George; Petropoulou, Evdokia N.; Zacharoulis, Achilleas

doi:10.1177/000331979905000507

Cited by 3 publications

(4 citation statements)

References 13 publications

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“…It is synthesized primarily in the zona glomerulosa of the adrenal gland via aldosterone synthase in response to elevated K + levels, volume depletion, and angiotensin II as part of the RAAS, regulating sodium and K + homeostasis in the distal renal tubule and collecting duct. In addition to the kidneys, aldosterone can also act on other tissues such as the myocardium, blood vessels, adipose tissue, and macrophages [14].…”

Section: Aldosteronementioning

confidence: 99%

“…In the kidney, the MR localizes to the distal tubules, collecting duct, podocytes, fibroblasts, and mesangial cells [30]. Once aldosterone binds to the MR, the new complex attaches to hormone response elements in the DNA, resulting in target gene transcription [14,30]. Although cortisol and other ligands also recognize the receptor with similar affinity, aldosterone is the principal steroid for MR activation [31].…”

Section: The Mrmentioning

confidence: 99%

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Mineralocorticoid Receptor-Associated Mechanisms in Diabetic Kidney Disease and Clinical Significance of Mineralocorticoid Receptor Antagonists

2023

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Background: Diabetic kidney disease (DKD) is a common disorder with multiple serious clinical implications, including an increased risk of end-stage kidney disease (ESKD), cardiovascular complications, heart failure, onset or worsening of hypertension, and premature death. Patients with DKD frequently require dialysis or kidney transplantation to manage their ESKD. Summary: Upregulation of the renin–angiotensin–aldosterone system is an important contributor to kidney disease progression, as highlighted by the results of trials evaluating angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in patients with albuminuria. Increasing evidence suggests the existence of a multidirectional network that involves aldosterone, the mineralocorticoid receptor (MR), and the Ras-related C3 botulinum toxin substrate 1 (Rac1) as driving forces in the generation of reactive oxygen species and oxidative stress-induced injury in the initiation of interstitial nephritis and eventual fibrosis in chronic kidney disease and DKD. The MR is a key element of this triangle, as highlighted by the beneficial effect of MR antagonists in preventing or reducing aldosterone- or Rac1-related effects in basic science studies, and the improved patient outcomes observed in clinical studies. Key Messages: Aldosterone can promote kidney disease in diabetes via the MR and via MR-independent actions through Rac1. However, the MR remains a key element of this triangle, with clinical data supporting the use of MR antagonists in delaying the progression of kidney disease in diabetes.

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Section: Aldosteronementioning

confidence: 99%

Section: The Mrmentioning

confidence: 99%

Mineralocorticoid Receptor-Associated Mechanisms in Diabetic Kidney Disease and Clinical Significance of Mineralocorticoid Receptor Antagonists

2023

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“…[24,26] The MR-mediated genomic activity begins to elicit effects within an hour after MR activation. [27] This biological effect is carried out by ion transporters and channels transcribed from MR-targeted genes. The major proteins in the kidney involved in maintaining the fluid and electrolyte balance include epithelial Na + Channel (ENaC), Na + /K+-ATPase pump, and serine/threonine kinase or serum/glucocorticoid-regulated kinase 1 (SGK1).…”

Section: Principle Behind Mineralocorticoid Receptor (Mr) Activationmentioning

confidence: 99%

Renoprotective Effects of Mineralocorticoid Receptor Antagonists Against Diabetic Kidney Disease

Bayne,

LeFevre,

Olstinske

et al. 2023

Advanced Biology

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Diabetic kidney disease (DKD) is a growing epidemic worldwide and a leading cause of end‐stage kidney disease. Mineralocorticoid receptor (MR) blockade using Finerenone is a recently approved therapeutic approach to slow down the progression of DKD in patients with type 2 diabetes in addition to other therapies such as angiotensin‐II converting enzyme inhibitors (ACEIs), angiotensin II receptor blockers (ARBs), sodium‐glucose co‐transporter 2 (SGLT2) inhibitors, and glucagon‐like peptide 1 (GLP‐1) analogs. This review elaborates on the pathophysiologic pathways activated by aldosterone (the human mineralocorticoid) in DKD, the pharmacology of three different generations of mineralocorticoid receptor antagonists (MRAs), specifically, spironolactone, eplerenone, and finerenone, and the mechanisms by which these MRAs elicit their protective effects on the kidney under diabetic settings.

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“…The possibility that myocardial ischemia can increase mortality in patients with HCM has been suspected on the basis of myocardial infarction at postmortem examination [5], the presence of ST-segment depression [6], and the higher incidence of perfusion defects on thallium scans in those with serious cardiac events [7-9]. The clinical significance and prognostic value of MB of the coronary arteries in patients with AHCM have been described only rarely [10-12]. This study aimed to determine the prevalence and prognostic significance of MB in patients with AHCM.…”

Section: Introductionmentioning

confidence: 99%

Clinical Outcomes of Myocardial Bridging versus No Myocardial Bridging in Patients with Apical Hypertrophic Cardiomyopathy

Zhai

Fan

An³

et al. 2018

Cardiology

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Objective: To determine the prevalence and clinical effects of myocardial bridging (MB) in patients with apical hypertrophic cardiomyopathy (AHCM). Methods: Angiograms from 212 AHCM patients were reviewed to identify MB. The patients were classified into 2 groups: AHCM with and AHCM without MB. We reviewed patient records on cardiovascular (CV) risk factors, symptoms, CV events, and CV mortality. Results: In all, 60 patients with MB and 100 without MB were included. Rates of angina (61.7 vs. 40%; p = 0.008), mimicking non-ST-segment elevation myocardial infarction (15 vs. 3%, p = 0.013), and Canadian Cardiovascular Society class III/IV angina (18.3 vs. 4%; p = 0.003) were higher in patients with MB than in those without. Mean follow-up periods (65.5 ± 50.5 vs. 64.4 ± 43.6 months, p = 0.378) and CV mortality (3.3 vs. 1%; p = 0.652) were similar in the 2 groups. Kaplan-Meier estimates demonstrated that CV event-free survival rates were lower in patients with MB than in those without (71.7 vs. 88%; p = 0.022). MB, late gadolinium enhancement, and female sex were independent risk factors for CV events in a multivariate Cox regression analysis adjusted for other risk factors. Conclusion: More serious symptoms and a higher risk of CV events were observed in AHCM patients with MB than in those without MB. CV mortality was similar in these 2 groups.

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Apical Hypokinesis in a Patient with Hypertrophic Cardiomyopathy and Myocardial Bridging: Reversal with Beta-Blockade

Cited by 3 publications

References 13 publications

Mineralocorticoid Receptor-Associated Mechanisms in Diabetic Kidney Disease and Clinical Significance of Mineralocorticoid Receptor Antagonists

Mineralocorticoid Receptor-Associated Mechanisms in Diabetic Kidney Disease and Clinical Significance of Mineralocorticoid Receptor Antagonists

Renoprotective Effects of Mineralocorticoid Receptor Antagonists Against Diabetic Kidney Disease

Clinical Outcomes of Myocardial Bridging versus No Myocardial Bridging in Patients with Apical Hypertrophic Cardiomyopathy

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