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The key clinical manifestations of Rheumatic heart disease (RHD) include several distinct cardiac symptoms.Carditis, a hallmark of acute rheumatic fever, involves inflammation of the heart's endocardium, myocardium, and pericardium. Chronic RHD often results from recurrent episodes of carditis. Its symptoms include the following:Murmurs are caused by valvular damage, especially to the mitral and aortic valves. Mitral stenosis or regurgitation is common, with characteristic heart murmurs...
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Rheumatic heart disease (RHD) management can be divided into two main strategies: prevention and long-term management.Primary PreventionPrimary prevention focuses on timely diagnosis and management of group A streptococcal pharyngitis to prevent acute rheumatic fever. The most widely used antibiotic for treating this condition is intramuscular benzathine penicillin G.Acute Rheumatic Fever TreatmentThe primary treatment goal for a patient diagnosed with acute rheumatic fever is to suppress the...
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Rheumatic Heart Disease I: Introduction01:23

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Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
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Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
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Clinical manifestationsPeripheral Arterial Disease (PAD) manifests through a range of symptoms, from the characteristic intermittent claudication to atypical presentations and severe complications in advanced stages. Intermittent claudication, a hallmark symptom of PAD, presents as exercise-induced muscle pain that typically resolves within minutes of rest. This pain is reproducible and stems from inadequate blood flow, leading to the accumulation of lactic acid produced during anaerobic...
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Calmodulinopathies: The Need for a Registry.

Peter J Schwartz1, Lia Crotti2

  • 1Istituto Auxologico Italiano IRCCS, Center for Cardiac Arrhythmias of Genetic Origin and Laboratory of Cardiovascular Genetics, Milano, Italy.

JACC. Clinical Electrophysiology
|September 3, 2025
PubMed
Summary
This summary is machine-generated.

Calmodulinopathies are rare genetic disorders linked to sudden cardiac death. Enrolling patients in the International Calmodulinopathy Registry is crucial for understanding disease mechanisms and improving patient management.

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Area of Science:

  • Cardiology
  • Genetics
  • Molecular Biology

Background:

  • Calmodulinopathies are rare genetic disorders with a high risk of sudden cardiac death.
  • Disease-causing variants in CALM genes lead to severe long QT syndrome, catecholaminergic polymorphic ventricular tachycardia, and idiopathic ventricular fibrillation.
  • Current knowledge relies on limited data from the International Calmodulinopathy Registry (ICamR), hindering progress.

Purpose of the Study:

  • To address the slow patient accrual in the ICamR.
  • To call for global physician participation in enrolling patients, including isolated cases.
  • To gather sufficient data for comprehensive genotype-phenotype correlation and improved risk stratification.

Main Methods:

  • A call to action for physicians worldwide to contribute patient data to the ICamR.
  • Leveraging existing knowledge from prior initiatives for long QT syndrome.
  • Establishing a collaborative registry for rare cardiac genetic disorders.

Main Results:

  • The current patient accrual in ICamR is insufficient for robust scientific inquiry.
  • A significant gap exists in understanding the full clinical spectrum and genotype-phenotype correlations.
  • Improved data collection is essential for advancing the management of calmodulinopathies.

Conclusions:

  • Increased patient enrollment in the ICamR is urgently needed.
  • Comprehensive data is vital for defining disease manifestations and guiding therapeutic strategies.
  • Global collaboration is key to advancing research in rare cardiac channelopathies like calmodulinopathies.