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Related Concept Videos

Pulmonary Hypertension: Classification and Pathogenesis01:30

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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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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...
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The cardiac conduction system produces and transmits electrical impulses that prompt myocardial contraction, ensuring efficient heart function. This intricate system ensures that the heart beats in a coordinated and efficient manner, beginning with the atria and then the ventricles. The conduction system optimizes cardiac output by maintaining this precise sequence, which is crucial for adequate blood circulation.
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Autorhythmicity is a term that refers to the heart's inherent ability to generate electrical signals and instigate muscle contractions. This self-regulating conduction system within the heart consists of two key components: the pacemaker cells and specialized conducting cells.
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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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Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
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Updated: Mar 10, 2026

Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice
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Atrioventricular Node Dysfunction and Ion Channel Transcriptome in Pulmonary Hypertension.

Ian P Temple1, Sunil Jit R J Logantha1, Mais Absi1

  • 1From the Institute of Cardiovascular Sciences (I.P.T., S.J.R.J.L., M.A., Y.Z., J.Y., A.A., M.P., G.M.Q., H.S., O.M., E.C., M.Z., A.M.G., G.H., M.R.B., H.D.) and School of Physics and Astronomy (S.C., H.Z.), University of Manchester, United Kingdom; School of Biomedical Sciences, University of Leeds, United Kingdom (E.P., M.D., E.W.); Kagawa Prefectural College of Health Sciences, Takamatsu, Japan (T.T.Y.); and Department of Medicine, University of California, San Francisco (V.S.M.).

Circulation. Arrhythmia and Electrophysiology
|December 17, 2016
PubMed
Summary
This summary is machine-generated.

Pulmonary hypertension causes heart block by altering the atrioventricular (AV) node

Keywords:
atrioventricular nodeechocardiographyheart blockion channelstranscriptome

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Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Medical Research

Background:

  • Heart block is a known complication of pulmonary hypertension.
  • The underlying mechanism linking these conditions remains unclear.
  • Investigating the atrioventricular (AV) node's ion channel transcriptome is crucial.

Purpose of the Study:

  • To test the hypothesis that heart block in pulmonary hypertension stems from changes in the AV node's ion channel transcriptome.
  • To elucidate the molecular basis of AV node dysfunction in pulmonary hypertension.

Main Methods:

  • Utilized the monocrotaline rat model for pulmonary hypertension.
  • Assessed cardiac function via echocardiography, ECG, and electrophysiology.
  • Quantified ion channel gene expression in the AV node using quantitative PCR.
  • Employed computer modeling to predict functional consequences of transcriptomic changes.

Main Results:

  • Monocrotaline injection induced pulmonary hypertension, right heart failure, and AV node dysfunction, including heart block.
  • Quantitative PCR revealed significant downregulation of key ion channel genes (Cav1.2/3, HCN1/2/4) in the AV node.
  • Computer modeling supported the link between transcriptomic alterations and heart block development.

Conclusions:

  • Pulmonary hypertension induces significant alterations in the AV node's ion channel transcriptome.
  • These transcriptomic changes are the likely cause of AV node dysfunction and heart block in pulmonary hypertension.