Changes in Right Ventricular Function with Exercise in Healthy Subjects: Optimal Parameters and Effects of Gender and Age.

BACKGROUND: Right ventricular (RV) function augments with exercise, and loss of this adaptive ability often determines symptoms. Reports on exercise-related changes in RV function in healthy subjects are sparse. In this study, healthy volunteers were prospectively recruited, and changes in RV function with exercise were examined, optimal parameters determined, and the effects of gender and age examined. METHODS: Treadmill exercise stress echocardiography with concurrent expired gas analysis was performed in 121 healthy volunteers. Parameters of RV systolic function (RV fractional area change, Doppler tissue s' velocity, and systolic strain and strain rate) and diastolic function (peak E and A velocity, Doppler tissue e', a' and early and late diastolic strain rate) were evaluated at baseline and after exercise, with the difference (Δ) being systolic and diastolic reserve. Changes in pulmonary arterial pressure (PAP) was measured when accurate estimation was possible. RESULTS: Most systolic functional parameters were augmented with exercise. However, systolic augmentation decreased with age (Δs': r = -0.31, P < .01; Δ strain: r = -0.28, P = .008; Δ systolic strain rate: r = -0.31, P < .01). Similar changes were observed with diastolic function (Δe': r = -0.33, P < .01; Δ early diastolic strain rate r = -0.20, P = .04). In the subgroup with PAP measurements, ΔPAP (r = 0.32, P < .01) increased with age. Men had greater augmentation of systolic reserve, but differences were negated when corrected for workload. S' velocity was the most robust measure of RV systolic function. CONCLUSIONS: There is a modest yet significant reduction in RV systolic and diastolic reserve with age, with an increase in PAP. S' velocity is a robust and feasible measure that should be considered given the increasing use of stress testing to evaluate RV function.

Circumflex coronary artery to left atrium fistula caused by mitral isthmus ablation.

Mitral isthmus ablation is an important component of catheter ablation for persistent atrial fibrillation and mitral isthmus dependent flutters. We describe a case where mitral isthmus ablation caused a fistula between the left circumflex artery and the left atrium and symptomatic ischaemia. The fistula was successfully closed with a covered stent.

Primary radiofrequency ablation of ventricular tachycardia early after myocardial infarction: evaluation in an ovine model.

BACKGROUND: Ventricular tachycardia (VT) is a significant complication of myocardial infarction. Radiofrequency ablation for postinfarct VT is reserved for drug refractory VT or VT storms. Our hypothesis is that radiofrequency ablation in the early postinfarct period could abolish or diminish late recurrences of VT. METHODS AND RESULTS: Myocardial infarct was induced by balloon occlusion of the left anterior descending artery in 35 sheep. The 25 survivors underwent programmed ventricular stimulation and electroanatomical mapping 8 days postinfarct. Animals with inducible VT (12 out of 25 animals) underwent immediate radiofrequency ablation. Further VT inductions were performed 100 and 200 days postinfarct. At day 8, 3.0±0.9 VT morphologies per animal were inducible. All were successfully ablated with 24±6 applications of radiofrequency energy. All had ablations on the left ventricular endocardium, and 67% had ablations on the right ventricular aspect of the interventricular septum. All targeted arrhythmias were successfully ablated acutely. One animal was euthanized because of hypotension from a serious pericardial effusion. The other 11 survived and remained arrhythmia free on subsequent inductions on the 100th and 200th days (P<0.001). The 13 animals without inducible VT remained noninducible at the subsequent studies. A historical control arm of 9 animals with inducible VT at day 8 remained inducible at day 100. CONCLUSIONS: Radiofrequency ablation on the eighth day after infarction abolished inducibility of VT at late induction studies ≤200 days in an ovine model. Early identification and ablation of VT after infarction may prevent or reduce late ventricular arrhythmias but needs to be validated in clinical studies.

Evolution of ventricular tachycardia and its electrophysiological substrate early after myocardial infarction: an ovine model.

BACKGROUND: Sudden arrhythmic death after myocardial infarction (MI) is most frequent in the first month. Early programmed ventricular stimulation (within 1 week) post-MI has been able to identify long-term ventricular tachycardia (VT) occurrence. We aimed to determine the timing of development and stabilization of VT circuits after MI and how the evolution of the underlying substrate differs with VT inducibility. METHODS AND RESULTS: MIs were induced in 36 sheep. The 21 survivors underwent serial electroanatomic mapping and programmed ventricular stimulation. Animals were classified as VTpos (inducible VT) or VTneg (noninducible VT) at day 8. Forty-three percent of MI survivors were VTpos on day 8 (9/21), and all remained inducible on day 100 with 1.5 (1.0-2.0) and 1.0 (1.0-2.0) morphologies per animal on days 8 and 100, respectively. Twelve-lead electrocardiogram matched in 15 of 19 VTs between days 8 and 100. The earliest presystolic ventricular activations during VT circuits were in similar locations at the 2 time points. The 12 VTneg animals remained noninducible on day 100. There was no difference in voltage or velocity substrate with time or inducibility. The area with fractionated signals increased with time and VT inducibility. VTpos animals had more linear regions of slowed conduction forming conducting channels. CONCLUSIONS: The inducibility and earliest presystolic endocardial activation sites of VT as well as voltage and velocity substrate on day 8 predicted those on day 100 postinfarct, indicating early formation and stabilization of the arrhythmogenic substrate. VT inducibility was influenced by the distribution of conducting channels and increased complex fractionated signals.

Direct transthoracic access to the left ventricle for catheter ablation of ventricular tachycardia.

BACKGROUND: Percutaneous approaches for radiofrequency ablation of ventricular tachycardia (VT) in the left ventricle are typically transarterial retro-aortic, antegrade transmitral via an interatrial septal puncture, or epicardial. However, all 3 approaches may be contraindicated in certain cases. We describe 2 cases of VT ablation in which aortic and mitral valve replacements did not permit utilization of any of these techniques. METHODS AND RESULTS: Direct access to the left ventricular cavity was achieved with a percutaneous puncture through the intercostal space overlying the apex in the first case and through a left minithoracotomy in the second. A sheath was then inserted via the Seldinger technique, allowing catheter access for mapping and ablation of the VT. After successful ablation, the sheaths were withdrawn and hemostasis was achieved. A large left hemothorax occurred from the left ventricular apical puncture in the first case. Direct closure with a purse-string suture in the second case achieved hemostasis. CONCLUSIONS: Direct percutaneous left ventricular puncture is a viable option for mapping and ablation of left ventricular VT. A minithoracotomy allows better hemostatic control. This technique has a role when other percutaneous approaches are contraindicated.