Components of left ventricular ejection and filling in patients with aortic regurgitation assessed by speckle-tracking echocardiography.

The aim of our study was to evaluate left ventricular (LV) longitudinal, radial, and rotational function and its relationship with conventional LV parameters of systolic and diastolic function in patients with aortic regurgitation (AR) by speckle-tracking echocardiography. MATERIAL AND METHODS. A total of 26 asymptomatic patients with moderate AR, 34 patients with severe AR, and 28 healthy controls were included into the study. LV rotation and longitudinal and radial strain were measured offline using speckle-tracking imaging. RESULTS. The systolic longitudinal strain (-18.3% [SD, 2.18%] vs. -21.0% [SD, 2.52%], P<0.05) and strain rate (-1.08 s(-1) [SD, 0.13 s(-1)] vs. -1.27 s(-1) [SD, 0.15 s(-1)], P<0.05) were significantly lower and apical rotation (11.3° [SD, 4.99°] vs. 8.30° [SD, 4.34°], P<0.05) as well as rotation rate (82.72°/s [SD, 28.24 °/s] vs. 71.00°/s [SD, 28.04 °/s], P<0.05) were significantly higher in the patients with moderate AR compared with the control patients. The LV systolic basal rotation, systolic radial strain, and diastolic radial strain rate were significantly reduced in the patients with severe AR compared with the control patients. The global longitudinal, radial strain, and LV systolic diameter were the independent predictors of LV ejection fraction in the patients with AR (R(2)=0.77). The LV systolic basal rotation in the control patients, diastolic longitudinal strain rate and systolic longitudinal strain in the patients with moderate and severe AR, respectively, were independent predictors of LV diastolic filling. CONCLUSIONS. LV long-axis dysfunction with an increased apical rotation was present in the patients with moderate AR, while LV radial function and systolic basal rotation were found to be reduced in more advanced disease. LV diastolic filling depended on diastolic and systolic LV strain and rotation components in the patients with AR.

The value of 99mTc-MIBI myocardial perfusion imaging in differentiation of heart failure conditioned by global left ventricular systolic impairment.

OBJECTIVE: The global left ventricular systolic impairment with left ventricular dilatation can manifest due to idiopathic dilated cardiomyopathy or ischemic heart disease and can present a similar clinical picture of severe heart failure. The aim of our investigation was to assess a differential diagnostic value of resting (99m)Tc-MIBI myocardial perfusion defects in evaluation of the etiology of heart failure. MATERIAL AND METHODS: The data of 2D echocardiography, coronary angiography, and myocardial gated single photon emission computed tomography with (99m)Tc-MIBI investigation were evaluated in 43 patients with global left ventricular systolic impairment, characterized by left ventricular end-diastolic diameter of > or =65 mm and ejection fraction of < or =40%. The idiopathic dilative cardiomyopathy was diagnosed in 26 patients (Group 1) and ischemic heart failure in 17 patients (Group 2). The area and the degree (severity) of myocardial perfusion defects (AMPD and DMPD) at rest in regions supplied by three coronary arteries were evaluated in all the patients. RESULTS: The area of perfusion defects in the left anterior descending (LAD) and right coronary artery (RCA) regions in dilative cardiomyopathy patients was smaller than in ischemic heart failure patients (1.43+/-0.9 vs 2.53+/-0.53, P=0.001, and 2.19+/-0.6 vs 2.82+/-0.56, P=0.02). The degree of perfusion defects was also less severe in the same circulation regions (1.39+/-0.93 vs 2.59+/-0.6, P=0.01, and 1.6+/-0.46 vs 2.71+/-0.15, P=0.001). We have designed a logistic regression model expressed by formula x=2.52AMPD(rca)+2.47AMPD(lad)+2.21DMPD(rca). Idiopathic dilative cardiomyopathy was predicted when x was < or =16 and ischemic heart failure when x was >16. The sensitivity in predicting idiopathic dilative cardiomyopathy was 94.44%, and the specificity was 88.24%. CONCLUSION: The difference in the area and degree of (99m)Tc-MIBI myocardial perfusion defects at rest in patients with heart failure caused by idiopathic dilative cardiomyopathy or ischemic heart failure is measurable and has a predictive value for differentiation of the etiology of global left ventricular systolic impairment.

Brain natriuretic peptide and other cardiac markers predicting left ventricular remodeling and function two years after myocardial infarction.

BACKGROUND: Left ventricular remodeling is a complex pathologic process of progressive left ventricular dilatation, leading to dysfunction and heart failure in patients after myocardial infarction. OBJECTIVE: To evaluate biochemical markers, reflecting cardiac remodeling process after first myocardial infarction and compare those markers with clinical characteristics of left ventricular remodeling. MATERIAL AND METHODS: Brain natriuretic peptide, troponin I, creatine kinase, creatine kinase MB mass, lactate dehydrogenase levels were measured in 30 patients with acute myocardial infarction on days 1, 2, 3-7 . Brain natriuretic peptide was measured at 3 months, 6 months, and 2 years after myocardial infarction. Echocardiographic parameters of left ventricular remodeling were determined in acute phase (day 1-3), at 3 months, 6 months, and 2 years after MI. RESULTS: In acute phase, brain natriuretic peptide level progressively increased according to worsening of left ventricular geometry: in normal left ventricle geometry group, brain natriuretic peptide level was 84.1 (58.7-121) pg/mL, in concentric remodeling group - 125 (69.2-165) pg/mL, in concentric hypertrophy group - 128 (74-368) pg/mL, and in eccentric hypertrophy group - 470 (459-494) pg/mL, P=0.02. Patients who had increased left ventricular end diastolic diameter index during 2-year period had higher brain natriuretic peptide level in the acute phase (584 (249-865) pg/mL vs. 120 (67-202) pg/mL, P=0.04) and also higher peak lactate dehydrogenase and troponin I levels. CONCLUSIONS: Brain natriuretic peptide level in acute phase of myocardial infarction is strongly associated with the markers of myocardial injury and related to left ventricular geometry changes and remodeling. Brain natriuretic peptide together with troponin I levels in acute phase of myocardial infarction might be useful in predicting subsequent cardiac function.

Prognostication of late left ventricular systolic dysfunction in patients with acute coronary syndrome during the acute period.

The aim of the study was to create the model of the combination of clinical and echocardiographic determinants during the acute period of acute coronary syndromes for the prognostication of the risk for left ventricular dysfunction after one year. We examined 565 patients with first-time acute coronary syndrome with no recurrence during one-year period. The studied group consisted of 496 patients, and the examined group--of 69 patients. All patients with acute coronary syndrome within the first three days underwent the evaluation of demographic, anamnesis, clinical indicators, risk factors for ischemic heart disease, ECG, and echocardiographic findings for the prognostication of the risk of left ventricular dysfunction after one year. Multiple logistic regression analysis was applied for the identification of independent determinants for the prognostication of left ventricular dysfunction, and three risk groups were identified. The prognostic informative value of the model was verified by comparing the incidence of left ventricular systolic dysfunction in risk groups after one year between the studied and the control groups. RESULTS. After one year, left ventricular systolic dysfunction (left ventricular ejection fraction <40%) in the presence of acute coronary syndrome remained in more than half (65.3%) of patients and returned to normal (left ventricular ejection fraction > or =40%) in one-third of patients (34.7%). Left ventricular systolic function that was normal during the acute period of coronary syndrome remained such in the majority (80.9%) of patients after one year, whereas one-fifth (19.1%) of patients developed left ventricular systolic dysfunction. The mathematical model for the prognostication of systolic dysfunction after one year was composed of the determinants of acute coronary syndrome: left ventricular ejection fraction <40%, anterior localization of Q-wave myocardial infarction, Killip class 3-4, left ventricular pseudo-normal or restrictive diastolic function, and frequent ventricular extrasystoles. The application of our model in the prognostication of late left ventricular systolic dysfunction during the acute period of coronary syndrome showed that the model was reliable, since after one year, the prognosticated left ventricular systolic dysfunction was determined in the majority (84.3%) of patients. The designed mathematical model is simple and is based on standard clinical and echocardiographic findings, and the scoring system allows for the prognostication of the risk for late left ventricular systolic dysfunction in any individual patient. The prognostication of the risk for late left ventricular systolic dysfunction during the acute period of coronary syndrome may help in the planning of treatment and outpatient care in patients with acute coronary syndrome.

Informative value of clinical markers for the risk of cardiovascular death in postinfarction chronic heart failure.

UNLABELLED: Symptomatic chronic heart failure (CHF) in patients with previous myocardial infarction results in a high risk of death. The aim of the study was to determine the informative value of different clinical markers and their combinations for cardiovascular death risk evaluation in case of CHF after Q-wave myocardial infarction (MI). METHODS: Two hundred and twenty-four patients with congestive heart failure NYHA class II-IV after Q-wave MI were followed-up for five years (median 2.6 +/- 2.0 years). The probability of cardiovascular death was evaluated using Kaplan-Meier curves, the impact of clinical variables on the risk of death, and adjusted risk of death were evaluated using Cox proportional regression method, and the total risk score of death was determined using the multivariate regression method. RESULTS: The probability of cardiovascular death within the first year was 21%, within two years 40%, within three years 55%, within four years 61%, and within five years 65%. According to the risk of death, the independent predictors were allotted a risk score which was determined for all patients and had shown a strong association with 5-year cardiovascular mortality. Patients with a risk score of 9, versus those with a score of 0, were found to have a 15-fold increase in cardiovascular mortality rate. CONCLUSION: The probability of cumulative cardiovascular mortality within five years in case of a symptomatic CHF after Q-wave MI was 65%. In the presence of risk factor combinations, the probability of death within three years reached 98%.

Brain natriuretic peptide and other cardiac markers in predicting left ventricular remodeling in patients with the first myocardial infarction.

UNLABELLED: Left ventricular remodeling is a complex pathologic process of progressive dilatation, leading to dysfunction and heart failure in patients with acute myocardial infarction. The aim of our study was to determine and evaluate biochemical markers, reflecting cardiac remodeling process in the patients with the first myocardial infarction and to compare those markers with clinical characteristics of left ventricular remodeling. MATERIAL AND METHODS: Concentrations of brain natriuretic peptide and markers of myocardial necrosis were measured on 1st , 2nd and 7th day after the onset of the first acute myocardial infarction, as well as after 3 and 6 months in 30 patients. Parameters of left ventricular remodeling were determined by echocardiographic investigation, which was performed in the acute phase and after 3 and 6 months. RESULTS: Brain natriuretic peptide concentration was found to be related to the left ventricular geometry in the acute phase: brain natriuretic peptide peak level was lower in the patients with the normal left ventricular geometry than in the patients with the changed left ventricular geometry (140.6+/-63.3 pg/ml vs. 385.7+/-283.9, p<0.05). Brain natriuretic peptide concentration in the acute phase was higher in the patients who had increased left ventricular end diastolic diameter through 6-month period (348.9+/-309.4 pg/ml vs. 145.1+/-109.6 pg/ml, p<0.05). Higher troponin I (58.8+/-33.6 ng/ml vs. 30.9+/-31.3 ng/ml, p<0.05) and troponin T (4.5+/-2.2 ng/ml vs. 1.9+/-2.0 ng/ml, p<0.05) levels were also associated with left ventricular dilatation through 6 months after myocardial infarction. CONCLUSIONS: Brain natriuretic peptide level in acute phase of myocardial infarction is related to the left ventricular geometry changes and remodeling. Brain natriuretic peptide together with other cardiac markers might be useful in predicting subsequent cardiac function.