Echocardiography Including Tissue Doppler Imaging Research Articles

Abstract 2746: Left Ventricular Diastolic Function Assessed By Tissue Doppler Echocardiography Is Impaired By β-blocker + Diuretic-based Therapy Compared With Calcium Antagonist + Ace Inhibitor-based Therapy: An ASCOT Substudy.

Background: Different anti-hypertensive therapies may vary in their effect on left ventricular diastolic function. The Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) randomized patients to β-blocker (atenolol) + diuretic (bendroflumethiazide-K)-based therapy (BB/D) or calcium antagonist (amlodipine) + ACE inhibitor (perindopril)-based therapy (CA/ACEI). We compared left ventricular diastolic function in the two treatment groups. Methods: Echocardiography including Tissue Doppler Imaging was performed on 977 subjects at two centres participating in ASCOT (St Mary’s Hospital, London, UK & Beaumont Hospital, Dublin, Eire) to assess left ventricular diastolic function after 12 months of treatment. Data are means (SD). Results: Systolic blood pressure (SBP) was similar in both treatment groups (BB/D = 137(17), CA/ACEI = 136(14); p = 0.3), but heart rate was significantly lower in BB/D group (BB/D = 57(10), CA/ACEI = 73(12); p<0.001). Ejection fraction did not differ between groups (BB/D = 69.5 (11.3)%, CA/ACEI = 69.2 (12.2)%, p = 0.8), but early diastolic mitral annular velocity (E’), a measure of diastolic relaxation, was significantly lower in BB/D group (BB/D = 7.9(1.8), CA/ACEI = 8.8 (2.0); p <0.001). E/E’, a measure of left ventricular filling pressure, was also significantly higher in BB/D group (8.1 (2.4) vs. 7.8 (2.1), p=0.01). Differences in E’ or E/E’ remained highly significant (<0.001) after adjustment for covariates (age, sex, fasting plasma glucose, body mass index and cholesterol). Further adjustment for SBP and heart rate had no impact on differences in mean E’ (p<0.001), but differences in E/E’ were attenuated. Conclusions: BB/D based therapy is associated with impaired diastolic function compared with CA/ACEI therapy. Differences in the effect of anti-hypertensive therapy on diastolic function could influence the risk of heart failure and other cardiovascular events in hypertensive patients with preserved systolic function.

Abstract 2690: Should We Classify Impaired Relaxation Pattern With Elevated E/e’ As Grade 1 Diastolic Dysfunction?

Purpose : Impaired relaxation pattern (grade 1 diastolic dysfunction) by Doppler echocardiography is known to reflect preserved left ventricular filling pressure (LVFP), while increased ratio of early diastolic transmitral flow velocity to mitral annular velocity (E/E’) indicated elevated LVFP. We evaluated the characteristics of impaired relaxation pattern with elevated E/E’ ratio. Methods : Eighty-eight patients (mean age 63 ± 11, 59 males) who had coronary artery disease with impaired relaxation pattern (E/A < 1) were enrolled. Echocardiography including tissue Doppler imaging (TDI) was performed. All patients underwent cardiac catheterization to investigate LV pre-A pressure (LVP pre-A ) within 6 hours after echocardiographic measurement. Patients were divided into subjects with E/E’ < 10 (n = 71) and E/E’ ≥ 10 (n = 17). Results : LVP pre-A was well correlated with echocardiographic Doppler and hemodynamic parameters (E/E’, r = 0.536, p < 0.001; LA volume, r = 0.295, p = 0.008; EF, r = -0.234, p = 0.028). Forty (45% of total) patients had high LVFP, defined as LVP pre-A ≥15 mmHg. Patients with E/E’ ≥10 had a significantly higher incidence of high LVFP, when compared to patients with E/E’ < 10 (88% vs 35%, p < 0.001). LA volume and LVP pre-A were significantly increased and EF was decreased in patients with E/E’ ≥ 10 (table 1 ). However, there were no significant differences of parameters derived from transmitral inflow and transpulmonary venous flow between two groups. Conclusions : In patients with impaired relaxation pattern, elevated E/E’ has related to elevation of LVFP, regardless of transmitral inflow and transpulmonary indices. Therefore, impaired relaxation pattern with elevated ratio of early diastolic transmitral flow velocity to mitral annular velocity (E/E’) may have been considered as another grade of diastolic dysfunction. Table 1

Cardiac abnormalities in adults with the attenuated form of mucopolysaccharidosis type I

SummaryBackground:Cardiac involvement in mucopolysaccharidosis type I (MPS I) has been studied primarily in its most severe forms. Cardiac involvement, particularly left ventricular (LV) systolic and diastolic function, in the attenuated form of MPS I is less well known.Methods:Cardiac function was prospectively investigated in 9 adult patients with the attenuated form of MPS I. All patients underwent 12-lead electrocardiography, 24 h Holter monitoring and two-dimensional echocardiography including tissue Doppler imaging (TDI). Eighteen age- and sex-matched healthy volunteers served as a control group.Results:Aortic, mitral and tricuspid valve thickening was seen in, respectively, 5 (56%), 4 (44%) and 2 (22%) patients. Moderate mitral valve stenosis was seen in 1 patient and moderate aortic stenosis in 2 patients. All patients had mild-to-moderate aortic and mitral valve regurgitation and 6 patients (67%) had mild-to-moderate tricuspid valve regurgitation. Despite normal LV dimensions, ejection fraction and mass index, MPS patients had lower mean systolic mitral annular velocities (6.1±0.6 vs 9.1±1.4 cm/s, p<0.01) compared to normal control subjects. Similarly, mean early diastolic mitral annular velocities were lower in MPS patients (7.8;±0.9 vs 13.3±3.3 cm/s, p<0.01).Conclusion:MPS I patients with the attenuated phenotype have not only valvular abnormalities but also LV diastolic and systolic abnormalities.

Reproducibility and clinical significance of exercise-induced increases in cardiac troponins and N-terminal pro brain natriuretic peptide in endurance athletes

Cardiac troponins I and T and brain natriuretic peptide are the accepted standards to serologically identify myocardial necrosis and elevated wall stress. In addition, they allow risk stratification in cardiovascular patients. The clinical significance of increases in cardiac markers after strenuous endurance exercise in obviously healthy athletes is unclear. We therefore examined the reproducibility and clinical significance of exercise-induced increases in cardiac troponins I and T and N-terminal pro brain natriuretic peptide after two standardized endurance exercise trials in healthy endurance athletes with prior competition-induced elevations of cardiac troponins (I, 0.08-1.93 mug/l; T, 0.01-0.56 mug/l). Twenty male athletes (36+/-7 years; VO2max: 60+/-5 ml/min per kg) completed a 1-h and a 3-h exercise study (exercise intensities 100 and 75%, respectively, of the individual anaerobic threshold) on two different days in randomized order to determine cardiac markers before, 30 min and 3 h after exercise. In addition to pre- and post-exercise echocardiography including tissue Doppler imaging, delayed enhancement magnetic-resonance-imaging was performed after a 3-h exercise study to detect myocardial necrosis. A marginal increase in cardiac troponin I was documented after both exercise trials (from 0.02 to 0.03 mug/l; P < 0.001). Cardiac troponin T remained without significant changes. N-terminal pro brain natriuretic peptide increased by 9 and 30 ng/l after 1-h and 3-h exercise studies, respectively (P < 0.001). In contrast to cardiac troponins, increases in N-terminal pro brain natriuretic peptide after competition correlated with those after 1-h exercise study (rho = 0.88) and 3-h exercise-study (rho = 0.82). No pathologies were demonstrated by echocardiography or delayed-enhancement magnetic resonance imaging. Due to the missing reproducibilty and evidence of myocardial damage, exercise-induced increases in cardiac troponins may represent a physiologic reaction under special conditions and seem to be without pathological significance in healthy athletes.

Evaluation of Subclinical Target Organ Damage for Risk Assessment and Treatment in the Hypertensive Patients

At some point in the natural history of hypertension, the compensatory increase in left ventricular mass ceases to be beneficial. Left ventricular hypertrophy (LVH) becomes a preclinical disease and an independent risk factor for congestive heart failure, ischemic heart disease, arrhythmia, sudden death, and stroke. In addition to elevated BP, several mechanisms are involved, including body size, age, gender, race, fibrogenic cytokines, and neurohumoral factors, notably angiotensin II, which favor interstitial collagen deposition and perivascular fibrosis. These tissue changes are responsible for the insidious contractile dysfunction that is associated with LVH, consequent to decreased coronary reserve and altered diastolic ventricular filling and relaxation. The cardinal investigations are echocardiography and electrocardiography. All antihypertensive drugs regress LVH, notably those that act on the renin-angiotensin-aldosterone system, which also could target the detrimental tissue changes. Regression enhances systolic midwall performance, normalizes autonomic function, and restores coronary reserve. The resulting improvement in prognosis has enshrined the detection, prevention, and reversal of LVH in the current guidelines of hypertension management.

A case of constrictive pericarditis presenting with protein-losing enteropathy

Constrictive pericarditis represents a rare cause of protein-losing enteropathy in children. Reported is an 11-year-old girl with protein-losing enteropathy (PLE) as the principal manifestations of constrictive pericarditis. After total pericardiectomy, symptoms and signs of PLE disappeared. Doppler echocardiography including tissue Doppler imaging is a useful noninvasive initial diagnostic tool for differential diagnosis of diastolic heart failure