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Pulmonary hypertension (PH) is a severe health condition in which the mean pulmonary arterial pressure increases to 25 mmHg or more, even when the body is at rest. This high pressure in the blood vessels that transport blood from the heart to the lungs can cause various symptoms, including shortness of breath, can lead to right heart failure, and significantly affect the overall quality of life.
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Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.
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Atrial fibrillation-a complex polygenetic disease.

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Atrial fibrillation (AF) genetics is complex, involving over 160 genes. Recent research highlights structural genes and atrial fibrosis, suggesting AF is more than an electrical disease, paving the way for new diagnostics and treatments.

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Area of Science:

  • Cardiology
  • Genetics
  • Molecular Biology

Background:

  • Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia, with significant epidemiological evidence pointing to a strong genetic influence.
  • Over 160 genes have been linked to AF, identified through linkage studies, functional analyses, and genome-wide association studies.
  • Traditionally viewed as an electrical disorder, emerging research suggests a broader etiological spectrum.

Purpose of the Study:

  • To review the genetic underpinnings of atrial fibrillation (AF).
  • To evaluate the contribution of both common and rare genetic variants to AF pathogenesis.
  • To explore the evolving understanding of AF, incorporating structural components and atrial cardiomyopathies.

Main Methods:

  • Review of landmark quantitative genetic studies and functional analyses.
  • Analysis of data from linkage studies and genome-wide association studies.
  • Synthesis of evidence implicating ion-channel, gap junction, transcription factor, and structural genes.

Main Results:

  • Rare variants in ion-channel, gap junction, and transcription factor genes are associated with AF.
  • Increasing evidence implicates structural genes in AF development.
  • Atrial fibrosis is more prevalent in AF patients, challenging the purely electrical disease model.

Conclusions:

  • The genetic basis of AF is multifaceted, involving a wide array of genes.
  • Atrial cardiomyopathies and structural changes play a crucial role in AF pathogenesis.
  • Future research into the genetic and structural basis of AF holds promise for improved diagnostic and therapeutic strategies.