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Sofie Verstreken

Publications and source records attributed to Sofie Verstreken.

5 recordsLinked to original sources
PubMed2006

Cardiac resynchronization therapy delays heart transplantation in patients with end-stage heart failure and mechanical dyssynchrony.

BACKGROUND: Cardiac dyssynchrony is frequent in advanced heart failure, and cardiac resynchronization therapy (CRT) may offer an alternative to heart transplantation. We aimed to investigate the impact of CRT on freedom from Tx and death in transplant candidates with end-stage heart failure. METHODS: Over a period of 2 years, 46 consecutive patients with refractory congestive heart failure due to dilated cardiomyopathy were referred for heart transplant evaluation. Patients with cardiac dyssynchrony > 107 milliseconds according to tissue Doppler imaging (TDI) or QRS duration > 150 milliseconds were treated with CRT (CRT group, n = 24), whereas patients without dyssynchrony were not treated (non-CRT group, n = 22). RESULTS: At baseline, both groups showed similar hemodynamic and functional parameters, including ejection fraction (19 +/- 10% vs 21 +/- 12%, not statistically significant [NS]) and Vo2max (11.9 +/- 2.0 vs 12.0 +/- 1.8 ml/kg/min, NS). After a follow-up of 488 +/- 346 days, cumulative survival with freedom from transplantation and death was higher in CRT vs non-CRT patients (92% vs 39%; p < 0.001). CRT patients showed a decrease in New York Heart Association (NYHA) class from 3.2 +/- 1.1 to 2.2 +/- 0.9 (p = 0.003) and an increase in Vo2max from 11.9 +/- 2.0 to 13.1 +/- 1.8 ml/kg/min (p = 0.02), and 71% (17 of 24) of these patients were successfully removed from the waiting list. CONCLUSIONS: In heart transplant candidates with significant dyssynchrony, CRT delays heart transplantation and improves NYHA class and exercise capacity. For these patients, CRT should be considered before heart transplantation.

Aged↗
PubMed2005

Non-invasive assessment of coronary flow reserve in idiopathic dilated cardiomyopathy: hemodynamic correlations.

BACKGROUND: Impaired vasodilator myocardial blood flow response has been observed in dilated cardiomyopathy (DCMP). However, the mechanisms responsible for this blunted response are not clear. In the present study, we investigated whether the blunted vasodilator flow response is related to indices of left ventricular performance in patients with idiopathic dilated cardiomyopathy. METHODS AND RESULTS: Eighteen DCMP patients and 12 healthy subjects (C) underwent transoesophageal echocardiography within 48 h from cardiac catheterization. Coronary flow velocity reserve (CFR) was measured in the proximal LAD as the ratio of the peak diastolic coronary flow velocity (Vd-M) after intravenous administration of adenosine to peak baseline diastolic flow velocity (Vd-R). Left ventricular (LV) mass index was positively correlated with baseline coronary diastolic velocity (r=0.415; p=0.043) and inversely correlated with coronary flow reserve (r=-0.570; p=0.003). The baseline coronary diastolic velocity was higher in DCMP vs C (56+/-13 cm/s vs 35+/-12 cm/s; p=0.04). In DCMP pts Vd-R positively correlated with end-diastolic wall stress (r=0.654; p=0.01). Vd increased in both C (96+/-32 cm/s; p<0.05 vs baseline) and DCMP patients (108+/-20 cm/s; p<0.01 vs baseline). The CFR was lower in DCMP patients vs C (1.93+/-0.78 vs 2.99+/-1.01; p=0.009). In DCMP pts CFR was negatively correlated with right atrial pressure (r=-0.595; p=0.015), LVEDP (r=-0.576; p=0.015), pulmonary capillary wedge pressure (PCWP: r=-0.772; p<0.001) and positively with ejection fraction (EF: r=0.683; p=0.003). CONCLUSION: Pts with DCMP have lower CFR compared to controls. This blunted CFR is due to higher baseline coronary flow and reflects higher wall stress. The close relation between CFR and EF, PCWP and LVEDP suggests that not only a higher baseline Vd but also compressive forces due to left ventricular dysfunction might be responsible for the observed blunted adenosine-mediated coronary vasodilation.

Adenosine↗
PubMed2005

Tailored echocardiographic interventricular delay programming further optimizes left ventricular performance after cardiac resynchronization therapy.

BACKGROUND: The aim of cardiac resynchronization therapy is correction of left ventricular (LV) dyssynchrony. However, little is known about the optimal timing of LV and right ventricular (RV) stimulation. OBJECTIVES: The purpose of this study was to evaluate the acute hemodynamic effects of biventricular pacing, using a range of interventricular delays in patients with advanced heart failure. METHODS: Twenty patients with dilated ischemic (n = 12) and idiopathic (n = 8) cardiomyopathy (age 66 +/- 6 years, New York Heart Association class III-IV, LV end-diastolic diameter >55 mm, ejection fraction 22% +/- 18%, and QRS 200 +/- 32 ms) were implanted with a biventricular resynchronization device with sequential RV and LV timing (VV) capabilities. Tissue Doppler echocardiographic parameters were measured during sinus rhythm before implantation and following an optimal AV interval with both simultaneous and sequential biventricular pacing. The interventricular interval was modified by advancing the LV stimulus (LV first) or RV stimulus (RV first) up to 60 ms. For each stimulation protocol, standard echocardiographic Doppler and tissue Doppler imaging (TDI) echo were used to measure the LV outflow tract velocity-time integral, LV filling time, intraventricular delay, and interventricular delay. RESULTS: The highest velocity-time integral was found in 12 patients with LV first stimulation, 5 patients with RV first stimulation, and 3 patients with simultaneous biventricular activation. Compared with simultaneous biventricular pacing, the optimized sequential biventricular pacing significantly increased the velocity-time integral (P <.001) and LV filling time (P = .001) and decreased interventricular delay (P = .013) and intraventricular delay (P = .010). The optimal VV interval could not be predicted by any clinical nor echocardiographic parameter. At 6-month follow-up, the incidence of nonresponders was 10%. CONCLUSION: Optimal timing of the interventricular interval results in prolongation of the LV filling time, reduction of interventricular asynchrony, and an increase in stroke volume. In patients with advanced heart failure undergoing cardiac resynchronization therapy, LV hemodynamics may be further improved by optimizing LV-RV delay.

Aged↗
PubMed2004

Wall stress modulates brain natriuretic peptide production in pressure overload cardiomyopathy.

OBJECTIVES: We postulated that both diastolic and systolic load modulate B-type natriuretic peptide (BNP) production in human pressure overload hypertrophy/failure. BACKGROUND: In isolated myocytes, diastolic stretch induces BNP messenger ribonucleic acid expression. However, the mechanism of the BNP release in human hypertrophy remains controversial. METHODS: In 40 patients with symptomatic aortic stenosis (AS), left ventricular (LV) performance and systolic and diastolic wall stress were calculated from combined invasive and echocardiographic data. Plasma BNP was determined by the rapid point-of-care bedside analyzer (Biosite Triage, Biosite Diagnostics Inc., San Diego, California). RESULTS: A significant relationship was observed between plasma BNP and pulmonary capillary wedge pressure (p < 0.001), fractional shortening (p = 0.001), and aortic valve area (p = 0.006). Furthermore, a significant correlation was noted between BNP and LV mass index (p = 0.005) as well as between BNP and markers of diastolic load such as LV end-diastolic wall stress (p = 0.011), indexed LV end-diastolic volume (p < 0.001), and isovolumic relaxation time (p = 0.02). Preoperative BNP levels were elevated in patients with AS compared with patients without AS. Plasma BNP was higher in AS patients with impaired versus normal preload reserve (297 +/- 56 pg/ml vs. 168 +/- 44 pg/ml; p = 0.017) and in AS patients with clinical deterioration after valve replacement compared with those without (399 +/- 82 pg/ml vs. 124 +/- 41 pg/ml; p = 0.011). CONCLUSIONS: In patients with AS, BNP appears to be regulated not only by systolic but also by diastolic load. This supports the hypothesis that myocardial stretch modulates BNP production in human pressure overload hypertrophy/failure.

Adult↗