Related Experiment Video

Updated: Jun 23, 2026

In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography
08:13

In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography

Published on: February 16, 2016

Cardiac troponin I is associated with impaired hemodynamics, progressive left ventricular dysfunction, and increased

Tamara B Horwich1, Jignesh Patel, W Robb MacLellan

  • 1Ahmanson-UCLA Cardiomyopathy Center, UCLA Division of Cardiology, 47-123 CHS, 10833 Le Conte Ave, Los Angeles, Calif 90095-1679, USA.

Circulation
|August 13, 2003
PubMed

Insights

Cardiac troponin I (cTnI) elevation in severe heart failure (HF) indicates worse hemodynamics and predicts increased mortality risk. Combining cTnI with B-type natriuretic peptide (BNP) further enhances prognostic value for HF patients.

Area of Science:

  • Cardiology
  • Biomarkers
  • Heart Failure Research

Background:

  • Cardiac troponin I (cTnI) is a key marker for myocardial injury, aiding diagnosis and prognosis in acute coronary syndromes.
  • Emerging evidence suggests elevated cTnI in severe heart failure (HF) may predict adverse outcomes.

Purpose of the Study:

  • To evaluate the association between cTnI levels and clinical parameters in advanced heart failure.
  • To determine if cTnI predicts mortality risk in patients with advanced HF.

Main Methods:

  • Assessed cTnI levels in 238 advanced HF patients referred for cardiac transplantation.
  • Excluded patients with acute myocardial infarction or myocarditis.
  • Correlated cTnI with B-type natriuretic peptide (BNP), hemodynamic profiles, and ejection fraction.

Main Results:

  • Detectable cTnI (≥0.04 ng/mL) was found in 49.1% of patients.
  • Detectable cTnI correlated with higher BNP, impaired hemodynamics (higher pulmonary wedge pressures, lower cardiac index), and declining ejection fraction.
  • Detectable cTnI was independently associated with a 2.05-fold increased mortality risk.
  • Combining cTnI and BNP improved prognostic value.

Conclusions:

  • cTnI is linked to hemodynamic compromise, elevated BNP, and worsening ventricular dysfunction in HF.
  • cTnI may serve as a novel biomarker for identifying high-risk HF patients.
  • cTnI, particularly with BNP, offers valuable prognostic information in advanced HF.
Abstract

More Related Videos

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats07:31

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats

Published on: December 2, 2016

Impact of High-intensity Interval Exercise and Moderate-Intensity Continuous Exercise on the Cardiac Troponin T Level at an Early Stage of Training07:40

Impact of High-intensity Interval Exercise and Moderate-Intensity Continuous Exercise on the Cardiac Troponin T Level at an Early Stage of Training

Published on: October 10, 2019

Related Concept Videos

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...
Imbalances in Cardiac Output01:26

Imbalances in Cardiac Output

The heart's primary function is to pump blood throughout the body, maintaining a balance between blood sent out (cardiac output) and blood returning (venous return). If this balance is disrupted, it can result in congestive heart failure (CHF), a severe condition where the heart becomes an inefficient pump, leading to inadequate blood circulation.
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send blood...
Blood Studies for Cardiovascular System I: Cardiac Biomarkers01:20

Blood Studies for Cardiovascular System I: Cardiac Biomarkers

Cardiac biomarkers are enzymes, proteins, and hormones released into the blood when cardiac cells are injured. They are powerful tools for triaging.
The essential diagnostic tools for detecting myocardial necrosis and monitoring individuals suspected of having acute coronary syndrome (ACS) include:
Troponins
Troponins, particularly cardiac troponins I and T, are the most precise and sensitive markers of myocardial injury. They are detectable within 4-6 hours of myocardial injury and remain...
Myocarditis I: Introduction01:21

Myocarditis I: Introduction

Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
Acute Coronary Syndrome III: Diagnostic Studies01:30

Acute Coronary Syndrome III: Diagnostic Studies

Diagnosing acute coronary syndrome or ACS begins with a thorough patient history. Notable symptoms include central, crushing chest pain radiating to the left arm, neck, jaw, or back, along with shortness of breath, sweating (diaphoresis), nausea, vomiting, dizziness, and palpitations.It is crucial to note any history of cardiac illnesses and assess risk factors, including age, gender, smoking, hypertension, diabetes, hyperlipidemia, and a sedentary lifestyle.During physical examination, vital...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

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...