Clinical Usefulness And Prognostic Value of Elevated Cardiac
Clinical Usefulness And Prognostic Value of Elevated Cardiac
Background: Right ventricular myocardial ischemia and injury contribute to right ventricular dysfunction and failure during acute pulmonary embolism. The objective of this study was to evaluate the clinical usefulness of cardiac troponin I (cTnI) in the assessment of right ventricular involvement and short-term prognosis in acute pulmonary embolism
Methods: Thirty-eight patients with acute pulmonary embolism were included in the study. Clinical characteristics, right ventricular involvement, and clinical outcome were compared in patients with elevated levels of serum cTnI versus patients with normal levels of serum cTnI.
Results: Among the study population (n = 38 patients), 18 patients (47%) had elevated cTnI levels (mean ± SD 1.6 ± 0.7 ng/mL, range 0.7-3.7 ng/mL, median, 1.4 ng/mL), and comprised the cTnI-positive group. In the other 20 patients, the serum cTnI levels were normal (≤0.4 ng/mL), and they comprised the cTnI-negative group. In the cTnI-positive group (n = 18 patients), 12 patients (67%) had right ventricular dilatation/hypokinesia, compared with 3 patients (15%) in the cTnI-negative group (n = 20 patients, P = .004). Right ventricular systolic pressure was significantly higher in the cTnI-positive group (51 ± 8 mm Hg vs 40 ± 9 mm Hg, P = .002). Cardiogenic shock developed in a significantly higher number of patients with elevated serum cTnI levels (33% vs 5%, P = .01). In patients with elevated cTnI levels, the odds ratio for development of cardiogenic shock was 8.8 (95% CI 2.5-21).
Conclusions: Patients with acute pulmonary embolism with elevated serum cTnI levels are at a higher risk for the development of right ventricular dysfunction and cardiogenic shock. Serum cTnI has a role in risk stratification and short-term prognostication in patients with acute pulmonary embolism.
Right ventricular dysfunction is a frequent consequence of severe pulmonary embolism, and correlates well with poor prognosis and higher mortality rates. The embolic obstruction and vasoconstriction of pulmonary arteries lead to an increase in pulmonary artery and right ventricular pressures and right ventricular dilatation in response to right ventricular pressure overload. An acute rise in pulmonary artery and right ventricular pressures and subsequent dilatation of the right ventricle may cause regional right ventricular ischemia and injury and, therefore, release cardiac troponin I (cTnI) without obstructive coronary artery disease. The field of cardiac biochemical markers is in a dynamic state, and in recent years, cardiac troponins have emerged as sensitive and specific markers for detecting myocardial injury, facilitating rapid bedside diagnosis and early risk stratification. Troponins I and T are the regulatory subunit of the troponin complex associated with the actin thin filament within muscle cells. Because cTnI is exclusively of cardiac origin and does not express in the skeletal muscle at any developmental stage, it has been shown to be highly specific for the detection of myocardial injury. This study was conducted to evaluate the clinical usefulness of cTnI in assessment of right ventricular involvement and short-term prognosis in acute pulmonary embolism.
Background: Right ventricular myocardial ischemia and injury contribute to right ventricular dysfunction and failure during acute pulmonary embolism. The objective of this study was to evaluate the clinical usefulness of cardiac troponin I (cTnI) in the assessment of right ventricular involvement and short-term prognosis in acute pulmonary embolism
Methods: Thirty-eight patients with acute pulmonary embolism were included in the study. Clinical characteristics, right ventricular involvement, and clinical outcome were compared in patients with elevated levels of serum cTnI versus patients with normal levels of serum cTnI.
Results: Among the study population (n = 38 patients), 18 patients (47%) had elevated cTnI levels (mean ± SD 1.6 ± 0.7 ng/mL, range 0.7-3.7 ng/mL, median, 1.4 ng/mL), and comprised the cTnI-positive group. In the other 20 patients, the serum cTnI levels were normal (≤0.4 ng/mL), and they comprised the cTnI-negative group. In the cTnI-positive group (n = 18 patients), 12 patients (67%) had right ventricular dilatation/hypokinesia, compared with 3 patients (15%) in the cTnI-negative group (n = 20 patients, P = .004). Right ventricular systolic pressure was significantly higher in the cTnI-positive group (51 ± 8 mm Hg vs 40 ± 9 mm Hg, P = .002). Cardiogenic shock developed in a significantly higher number of patients with elevated serum cTnI levels (33% vs 5%, P = .01). In patients with elevated cTnI levels, the odds ratio for development of cardiogenic shock was 8.8 (95% CI 2.5-21).
Conclusions: Patients with acute pulmonary embolism with elevated serum cTnI levels are at a higher risk for the development of right ventricular dysfunction and cardiogenic shock. Serum cTnI has a role in risk stratification and short-term prognostication in patients with acute pulmonary embolism.
Right ventricular dysfunction is a frequent consequence of severe pulmonary embolism, and correlates well with poor prognosis and higher mortality rates. The embolic obstruction and vasoconstriction of pulmonary arteries lead to an increase in pulmonary artery and right ventricular pressures and right ventricular dilatation in response to right ventricular pressure overload. An acute rise in pulmonary artery and right ventricular pressures and subsequent dilatation of the right ventricle may cause regional right ventricular ischemia and injury and, therefore, release cardiac troponin I (cTnI) without obstructive coronary artery disease. The field of cardiac biochemical markers is in a dynamic state, and in recent years, cardiac troponins have emerged as sensitive and specific markers for detecting myocardial injury, facilitating rapid bedside diagnosis and early risk stratification. Troponins I and T are the regulatory subunit of the troponin complex associated with the actin thin filament within muscle cells. Because cTnI is exclusively of cardiac origin and does not express in the skeletal muscle at any developmental stage, it has been shown to be highly specific for the detection of myocardial injury. This study was conducted to evaluate the clinical usefulness of cTnI in assessment of right ventricular involvement and short-term prognosis in acute pulmonary embolism.
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