Cardiac resynchronization therapy plus coupled pacing improves acutely myocardial function in heart failure patients.

BACKGROUND: Coupled pacing (CP), which consists of an additional beat delivered after ventricular refractory period, has been proposed to reduce ventricular rate and increase ventricular contractility. We hypothesized that CP may be added to cardiac resynchronization therapy (CRT) to improve CRT effect in heart failure (HF) patients. METHODS: The study included 20 consecutive HF patients in sinus rhythm referred for CRT-defibrillator (CRT-D) implantation (baseline left ventricular ejection fraction [LVEF] 27 ± 6%, baseline QRS duration 149 ± 33 ms, age = 63 ± 11 years). CP associated with CRT (CRT + CP) was delivered during CRT-D implantation from the right and left ventricular leads simultaneously. Echocardiography data were collected at baseline, during CRT and CRT + CP to assess changes in LVEF, cardiac output (CO), longitudinal global strain assessed by speckle tracking, and LV dyssynchrony (opposing wall delay using tissue Doppler imaging). RESULTS: Compared to the conventional CRT, heart rate (HR) markedly decreased during CRT + CP (79 ± 20 beats/min vs 51 ± 8 beats/min, P < 0.0001) and was associated with a significant increase in LVEF (30 ± 8% vs 35 ± 8%, P = 0.0002) and peak of longitudinal global strain (-6 ± 2% vs -8 ± 2%, P < 0.0001). Importantly, during CRT + CP, CO increased (3.8 ± 1.0 L/min vs 4.4 ± 1.4 L/min, P = 0.004) and cardiac synchronicity remained unchanged (38 ± 24 ms for CRT alone vs 27 ± 18 ms for CRT + CP, P = 0.1). CONCLUSION: In sinus rhythm HF patients, acute CP application in addition to CRT decreases HR and contributes to myocardial contractility and CO improvement without deleterious impact on ventricular synchronicity.

Left ventricular dyssynchrony and 2D and 3D global longitudinal strain for differentiating physiological and pathological left ventricular hypertrophy.

BACKGROUND: Diagnosis of hypertrophic cardiomyopathy (HCM) in athletes can be challenging. AIMS: To ascertain parameters that differentiate patients with HCM from athletes with moderate left ventricular (LV) hypertrophy (LVH 13-15mm). METHODS: We retrospectively included 100 men: 50 elite rugby players (25 with moderate LVH and 25 with no LVH), 25 patients with HCM and moderate LVH and 25 controls. LV dyssynchrony was defined as the standard deviation of time to peak 2D longitudinal strain (16-segment model) and global strain components were computed from two- (2D) and three-dimensional (3D) speckle tracking. RESULTS: 2D global longitudinal strain (GLS) (18±2% vs. 19±2%) and various 3D strain components were similar in athletes with moderate LVH and controls, while LV volumes and dyssynchrony (39±8 vs. 31±9ms; P<0.001) were greater in athletes with moderate LVH. The accuracy for differentiating patients with HCM from athletes ranged between 0.57 and 0.92 for various markers, with the best obtained for LV dyssynchrony (AUC=0.92;>48ms had sensitivity=83%, specificity=89%). Binary logistic regression showed that accuracy was improved when LV dyssynchrony was combined with 2D GLS. HCM was excluded when 2D GLS was preserved (>18%) and there was no LV dyssynchrony (>48ms) and only patients with HCM had reduced longitudinal strain and LV dyssynchrony. CONCLUSIONS: LV dyssynchrony combined with GLS can be used to differentiate athletes with moderate LVH from patients with HCM.

Hemodynamic effects of Ivabradine in addition to dobutamine in patients with severe systolic dysfunction.

BACKGROUND: Dobutamine induced tachycardia increases myocardial oxygen consumption and impairs ventricular filling. We hypothesized that Ivabradine may be efficient to control dobutamine induced tachycardia. METHODS: We assessed the effects of Ivabradine in addition to dobutamine in stable heart failure (HF) patients (LVEF < 35%, n = 22, test population) and validated its effects in refractory cardiogenic shock patients (n = 9, validation population) with contraindication to cardiac assistance or transplant. In the test population (62 ± 17 years, LVEF = 24 ± 8%), systolic and diastolic function were assessed at rest and under dobutamine [10 γ/min], before and after Ivabradine [5mg per os]. In the validation population (54 ± 11 years, LVEF = 22 ± 7%), Ivabradine [5mg twice a day] was added to the dobutamine infusion. RESULTS: In the test population, Ivabradine decreased heart rate [HR] at rest and during dobutamine echocardiography (-9 ± 8 bpm, P = 0.0004). The decrease in HR was associated with a decrease in cardiac power output and an increase in diastolic duration at rest (+ 74 ± 67 ms, P = 0.0002), and during dobutamine infusion (+ 75 ± 67 ms, P < 0.0001). Change in LVEF during dobutamine was greater after Ivabradine treatment than before (+ 7.2 ± 4.7% vs. + 3.6 ± 4.2%, P = 0.002). In the validation population, Ivabradine decreased HR (-18 ± 11 bpm, P = 0.008) and improved diastolic filling time (+ 67 ± 42 ms, P = 0.012) without decreasing cardiac output. At 24h, Ivabradine improved systolic blood pressure (+ 9 ± 5 mmHg, P = 0.007), daily urine output (+ 0.7 ± 0.5L, P = 0.008), oxygen balance (ΔScv02 = + 13 ± 15%, P = 0.010), and NT-pro BNP (-2270 ± 1912 pg/mL, P = 0.017). Finally, only 2/9 (22%) patients died whereas expected mortality determined from a historical cohort was 78% (P = 0.017). CONCLUSION: This pilot study demonstrates the safety and potential benefit of a HR lowering agent in cardiogenic shock.