Cardiac transplantation in a patient with emotionally triggered implantable cardioverter defibrillator storms

The implantable cardioverter defibrillator (ICD) may be responsible for psychological disorders especially among patients experiencing multiple shocks. An associated hyperadrenergic state (e.g., anger, anxiety) may trigger malignant ventricular arrhythmias repeatedly treated by ICD shocks, entertaining a "vicious circle” often difficult to interrupt. Despite aggressive cardiac and psychological therapeutic efforts, this condition may be refractory, finally leading to heart transplantation, as described in this case repor

Toward understanding response to cardiac resynchronisation therapy

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The shape of the aortic outflow velocity profile revisited: is there a relation between its asymmetry and ventricular function in coronary artery disease?

AIMS: Myocardium contracts in the beginning of ejection causing outflow acceleration, resulting in asymmetric outflow velocity profiles peaking around one-third of ejection and declining when force development declines. This article aimed to demonstrate that decreased contractility in coronary artery disease (CAD) changes outflow timing and profile symmetry. ----- METHODS AND RESULTS: Seventy-nine patients undergoing routine full dose dobutamine stress-echo (DSE) were divided into two groups based on resting wall motion and DSE response: DSE negative (DSE(neg)) (35 of 79 patients) and positive (DSE(pos)) (44 of 79 patients) which were compared with 32 healthy volunteers. Aortic CW-Doppler traces at rest were analysed semi-automatically; time-to-peak (T(mod)), ejection-time (ET(mod)), rise-time (t(rise)), and fall-time (t(fall)) were quantified. Asymmetry (asymm) was calculated as the normalized difference of left and right half of the spectrum. Normal curves were triangular, early-peaking, whereas patients showed more rounded shapes and later peaks. T(rise) was longest in DSE(pos). T(fall) was shortest in DSE(pos), followed by controls and DSE(neg). Asymm was lowest in DSE(pos), followed by controls and DSE(neg). Abnormally symmetric profiles (asymm <0.25) were found in none of the controls, 2.9% DSE(neg), and 27.3% DSE(pos). A good correlation was found between assym and ejection fraction (EF) and T(mod)/ET(mod) and EF. Notably, an LV dynamic gradient was induced in 71.4% DSE(neg) and in 18.2% DSE(pos), associated with LV hypertrophy and supernormal (very asymmetric) traces. ----- CONCLUSION: Decreased myocardial function results in a more symmetrical outflow, while very asymmetrical traces suggest increased contractility, potentially inducing intra-cavity gradients during DSE. Therefore, including outflow symmetry as a clinical measurement provides additional information on patients with CAD

The shape of the aortic outflow velocity profile revisited: is there a relation between its asymmetry and ventricular function in coronary artery disease?

Aims Myocardium contracts in the beginning of ejection causing outflow acceleration, resulting in asymmetric outflow velocity profiles peaking around one-third of ejection and declining when force development declines. This article aimed to demonstrate that decreased contractility in coronary artery disease (CAD) changes outflow timing and profile symmetry. Methods and results Seventy-nine patients undergoing routine full dose dobutamine stress-echo (DSE) were divided into two groups based on resting wall motion and DSE response: DSE negative (DSE neg ) (35 of 79 patients) and positive (DSE pos ) (44 of 79 patients) which were compared with 32 healthy volunteers. Aortic CW-Doppler traces at rest were analysed semi-automatically; time-to-peak (T mod ), ejection-time (ET mod ), rise-time (t rise ), and fall-time (t fall ) were quantified. Asymmetry (asymm) was calculated as the normalized difference of left and right half of the spectrum. Normal curves were triangular, early-peaking, whereas patients showed more rounded shapes and later peaks. T rise was longest in DSE pos . T fall was shortest in DSE pos , followed by controls and DSE neg . Asymm was lowest in DSE pos , followed by controls and DSE neg . Abnormally symmetric profiles (asymm ,0.25) were found in none of the controls, 2.9% DSE neg , and 27.3% DSE pos . A good correlation was found between assym and ejection fraction (EF) and T mod /ET mod and EF. Notably, an LV dynamic gradient was induced in 71.4% DSE neg and in 18.2% DSE pos , associated with LV hypertrophy and supernormal (very asymmetric) traces. Conclusion Decreased myocardial function results in a more symmetrical outflow, while very asymmetrical traces suggest increased contractility, potentially inducing intra-cavity gradients during DSE. Therefore, including outflow symmetry as a clinical measurement provides additional information on patients with CAD

Toward understanding response to cardiac resynchronization therapy: left ventricular dyssynchrony is only one of multiple mechanisms.

International audienceAIM: To date, most published echocardiographic methods have assessed left ventricular (LV) dyssynchrony (DYS) alone as a predictor for response to cardiac resynchronization therapy (CRT). We hypothesized that the response is instead dictated by multiple correctable factors. METHODS AND RESULTS: A total of 161 patients (66 +/- 10 years, EF 24 +/- 6%, QRS > 120 ms) were investigated pre- and post-CRT (median of 6 months). Reduction in NYHA Class >/=1 or LV reverse remodelling (end-systolic volume reduction >/= 10%) defined response. Four different pathological mechanisms were identified. Group1: LVDYS characterized by a pre-ejection septal flash (SF) (87 patients, 54%). Elimination of SF (77 of 87 patients) resulted in reverse remodelling in 100%. Group 2: short-AV delay (21 patients, 13%) resolution (19 of 21 patients) resulted in reverse remodelling in 16 of 19. Group 3: long-AV delay (16 patients, 10%) resolution (14 of 16 patients) resulted in NYHA Class reduction >/=1 in 11 with reverse remodelling in five patients. Group 4: exaggerated LV-RV interaction (15 patients, 9%) reduced post-CRT. All responded clinically with fall in pulmonary artery pressure (P = 0.003) but did not volume respond. Group 5: patients with none of the above correctable mechanisms (22 patients, 14%). None responded to CRT. CONCLUSION: CRT response is dictated by correction of multiple independent mechanisms of which LVDYS is only one. Long-axis DYS measurements alone failed to detect 40% of responders