Left ventricular mechanics during right ventricular apical or left ventricular-based pacing in patients with chronic atrial fibrillation after atrioventricular junction ablation

OBJECTIVES: The aim of the study was to evaluate whether left ventricular (LV) mechanics are better under LV-based pacing than under right ventricular (RV) apical pacing in patients with permanent atrial fibrillation (AF) after atrioventricular junction (AVJ) ablation. BACKGROUND: "Ablate and pace" is an acceptable therapy for drug-refractory AF. However, the RV apical stimulation commonly used seems to interfere with the beneficial hemodynamic effect of regularization of heart rhythm. METHODS: The study included 12 patients (5 men, mean age 62 +/- 8.3 years), 6 with impaired and 6 with normal LV systolic function. All of them had a biventricular pacemaker system implanted and underwent atrioventricular node ablation for drug-refractory chronic AF. Using a conductance catheter, we analyzed LV pressure-volume loops during routine coronary angiography in order to evaluate short-term changes in LV mechanics during RV apical and LV-based (LV free wall or biventricular) pacing. RESULTS: Compared with RV pacing, LV-based pacing significantly improved the indexes of LV systolic function (i.e., end-systolic pressure and volume, cardiac index, stroke work, preload recruitable stroke work, maximal rate of rise of LV pressure [dP/dt(max)], LV ejection fraction, and end-systolic elastance). The LV diastolic filling indexes, end-diastolic pressure and volume, were better during LV-based pacing, whereas LV diastolic function indexes, -dP/dt(max), passive diastolic chamber stiffness, and time constant of LV isovolumic relaxation showed no clear change. CONCLUSIONS: In the short term, LV-based pacing is superior to RV apical pacing in terms of contractile function and LV filling after AVJ ablation for drug-refractory AF.     

Differentiation between late potentials of right ventricular and of left ventricular origin

The aim of this study was to determine whether late potentials of right and left ventricular origin could be differentiated with the use of a signal-averaging technique. Nineteen patients with both late potentials and recurrent sustained ventricular tachycardia were divided into 2 groups according to the origin of their late potentials. Group I consisted of 10 patients with late potentials that originated from the right ventricle. Group II consisted of 9 patients with late potentials originating from the left ventricle. Signal-averaged electrocardiograms (Marquette Electronics MAC I unit) were recorded using 3 bipolar and 3 augmented unipolar leads (the electrode positions were V1, V5 and V6R) with a band-pass filter of 100 to 300 Hz. The augmented unipolar V5 lead (aV5) was used for left-side recording and the augmented unipolar V1 lead (aV1) was used for right-side recording. In group I, the mean maximal late potential amplitude was larger in lead aV1 than in lead aV5 (5.1 +/- 2.5 vs 3.7 +/- 1.8 microV, p less than 0.005) and the maximal late potential amplitude was larger in lead aV1 in all except 1 patient. In group II, however, the mean maximal late potential amplitude was smaller in lead aV1 than in lead aV5 (4.0 +/- 3.0 vs 5.7 +/- 3.2 microV, p less than 0.005) and the maximal late potential amplitude was smaller in lead aV1 in all patients. Thus, the origin of late potentials (right ventricular vs left ventricular origin) can be determined by comparing the maximal amplitudes of late potentials in the right- and left-sided leads. This method might be useful in determining ventricular tachycardia origins.     

A left ventricular epicardial to right ventricular endocardial dominant frequency gradient exists in human ventricular fibrillation

Purpose  

We hypothesized that in patients with left ventricular dysfunction undergoing implant of a biventricular ICD, the local dominant frequency during early induced ventricular fibrillation would be higher at an epicardial left ventricular position compared to an endocardial right ventricular position.     

Treatment of perinfarction recurrent ventricular fibrillation by percutaneous pharmacological block of left stellate ganglion

A patient suffering from an acute myocardial infarction presented on the seventh and eighth days of hospitalization recurrent episodes of ventricular fibrillation refractory to antiarrhythmic treatment. The life-threatening ventricular fibrillation was suppressed by percutaneous pharmacological block of the left stellate ganglion.     

Idiopathic verapamil-sensitive left ventricular tachycardia complicated by right ventricular outflow tract ventricular tachycardia and ventricular fibrillation.

Idiopathic ventricular tachycardias (VTs) are generally divided into those arising from the right ventricle and those arising from the left ventricle. There has been few reports of two morphologically distinct VT occurring in patients with no apparent structural heart disease. We report a patient with verapamil-sensitive left VT with a right bundle branch block pattern that spontaneously changed to VT with a left bundle branch block pattern. Ventricular fibrillation was induced by the application of programmed stimulation. Although it is unclear if our patient with pleomorphic VT has ventricular vulnerability, it is necessary to investigate further and follow him carefully.     

Prevention of late postmyocardial infarction left ventricular remodeling: An update

Cardiac remodeling remains an important primary therapeutic target in patients with myocardial infarction (MI) and chronic heart failure. It also has utility as a reliable surrogate for clinical outcomes. The past three decades of research have demonstrated the importance of cardiac remodeling as a basic mechanism in the progression of heart failure. Novel therapeutic advances have allowed more patients to survive acute MI. Strategies to prevent or halt adverse left ventricular remodeling have included pharmacotherapy, percutaneous interventions, device-based therapies, and surgical procedures. More recently, experimental research has added opportunities for novel approaches to prevent and reverse cardiac remodeling. This review summarizes the effects of current and future therapeutic strategies on left ventricular remodeling and dysfunction after MI.     

Prevention of left ventricular remodeling after myocardial infarction

Opinion statement Postinfarction left ventricular remodeling begins early after acute myocardial infarction and may continue for months to years afterward. Early re-establishment of flow in the occluded artery is associated with smaller left ventricular cavity volumes and reduced remodeling. Acute percutaneous coronary intervention (PCI) or thrombolytic therapy (for patients more than 1 hour away from a catheterization facility) as early as possible after symptoms is critical. Late reperfusion (PCI more than 12 hours after infarction) may prove useful, and this will be determined by the results of ongoing clinical trials. Recurrent MI is reduced by antiplatelet agents (aspirin in most patients) and by 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors. Intravenous nitroglycerin may limit early (initial 24 hours) dilatation following infarction, but long-term use in asymptomatic patients is not efficacious. Betaadrenergic receptor antagonists and angiotensin-converting enzyme (ACE) inhibitors have independent efficacy in attenuating the early and late phases of remodeling. The combined use of a beta-blocker and an ACE inhibitor has greater efficacy than either agent alone, provided they are tolerated hemodynamically. Although angiotensin II receptor antagonists have similar efficacy to ACE inhibitors and have fewer side effects, the angiotensin II receptor blockers should be reserved for patients intolerant to ACE inhibitors. In patients requiring diuretic therapy, spironolactone is preferred because of its salutary properties regarding extracellular matrix remodeling, specifically in reducing fibrosis. Surgical revascularization with or without associated mitral valve repair is useful in selected patients with severe ischemic mitral regurgitation or hibernating myocardium. New therapies directed at modulating the remodeling process may focus on manipulating the components of the extracellular matrix to reduce the deleterious impact of this process.     

Heterogeneity of left ventricular signal characteristics in response to acute vagal stimulation during ventricular fibrillation in dogs

Studies have shown that long-term vagal stimulation is protective against ventricular fibrillation; however, the effects of acute vagal stimulation during ventricular fibrillation in the normal heart have not been investigated. We examined the effects of acute vagal stimulation on ventricular fibrillation in a canine model. In 4 dogs, we induced 30-second periods of ventricular fibrillation by means of intraventricular pacing. During 2 of the 4 periods of fibrillation that we analyzed, vagal stimulation was delivered through electrodes in the caudal ends of the vagus nerves. Noncontact unipolar electrograms were recorded from 3 ventricular regions: the basal septum, apical septum, and lateral free wall. We then computed the most frequent cycle length, mean organization index, and mean electrogram amplitude for each region. During fibrillation, vagal stimulation shortened the most frequent cycle lengths in the basal septum (P=0.02) and apical septum (P=0.0001), but not in the lateral wall (P=0.46). In addition, vagal stimulation significantly reduced the mean organization indices in the apical septum (P <0.001) and lateral wall (P <0.001), but not in the basal septum (P=0.19). Furthermore, vagal stimulation raised the mean electrogram amplitude in the basal septum (P <0.01) but lowered it substantially in the apical septum (P=0.00005) and lateral wall (P=0.00003). We conclude that vagal stimulation acutely affects the characteristics of ventricular fibrillation in canine myocardium in a spatially heterogeneous manner. This nonuniformity of response may have implications with regard to manipulating the autonomic system as a means of modifying the substrate for ventricular dysrhythmias.     

Similar left and right ventricular sarcomere structure after support with a left ventricular assist device suggests the utility of right ventricular biopsies to monitor left ventricular reverse remodeling

BACKGROUND: To evaluate whether the morphology of the contractile filaments in cardiomyocytes of patients with end-stage heart failure, treated with a left ventricular assist device (LVAD), is identical in the left- and right ventricle (LV, RV) and in the interventricular septum (IVS) and can be monitored by biopsies taken with a bioptome. The application of an LVAD as a bridge to recovery of cardiac function requires monitoring of myocyte recovery. The use of RV biopsies for this purpose might be feasible, if morphologic findings in the RV coincide with those in the LV. METHODS AND RESULTS: At the time of heart transplantation, myocardial biopsies of LV, RV and IVS from 13 patients after LVAD support were compared using immunohistochemistry with monoclonal antibodies against contractile proteins. Additionally, in five of these patients, small biopsies obtained with a diagnostic bioptome were compared with large transmural biopsies of the same region. Hemodynamic monitoring was performed when the patients were fully recovered from the implantation, to rule out persistent RV failure. The staining pattern of actin, myosin, tropomyosin, troponin T and C was identical in the biopsies of LV, RV and IVS. Small biopsies taken with a bioptome appeared to be representative for the larger biopsies. Hemodynamic monitoring showed absence of RV failure in our study group. CONCLUSION: In the absence of RV failure, morphology of the contractile myofilaments after LVAD support for 215+/-143 days is identical in LV, RV and IVS. This may allow monitoring of the possible occurrence of LV reverse remodeling by RV biopsies.     

Dual-site right ventricular and left ventricular pacing in a patient with left ventricular systolic dysfunction and atrial fibrillation using a standard CRT-D device

In patients undergoing cardiac resynchronization therapy with defibrillator (CRT-D) implantation for left ventricular systolic dysfunction (LVSD) accompanied by permanent atrial fibrillation (AF), generally, the unused atrial port is plugged at device implantation. We describe an alternative use for the atrial-port in this case report.A 43 year old gentleman with LVSD due to left ventricular non-compaction (LVNC) and AF of unknown duration underwent a CRT-D implantation after optimization of cardiac failure treatment. The atrial-port which would otherwise have been plugged was connected to a high right ventricular septal (RVS) pacing-lead and the shock-lead was positioned at the right ventricular apex (RVA). This approach permitted modified cardiac resynchronization in a high RVS to left ventricular (LV) and RVA pacing sequence using the high RVS and LV pacing combined with a shock vector including the RV apex. A standard CRT-D device with a minimum programmable A–V delay of 30 ms (technically RVS to LV delay in the ‘DDD’ pacing mode) was used. The device was programmed to a ‘DDD’ pacing mode (sequential multi-site ventricular pacing with some programmability). The mode switch operation was programmed ‘OFF’ since atrial sensing is unavailable. Device-delivered shocks did not cardiovert the patient back to sinus rhythm suggesting that the AF was permanent (no prior cardioversion attempts were made on the presumption that the chances of maintaining sinus rhythm, given the underlying cardiac condition, were low). Subsequently, the patient required radio-frequency ablation of the atrio-ventricular node for conducted AF. Symptomatic, echocardiographic and radiological improvement preceded atrio-ventricular node ablation.ConclusionAmongst AF patients with permanent AF undergoing CRT-D implantation, those patients who are likely to have the CRT-D device atrial-ports plugged could benefit from having both the options of (i) a RVA shock vector as well as (ii) a high RVS-pacing feasible, by utilizing the atrial-port of a conventional CRTD device for a RVS pacing lead, should a RVA shock-lead position be preferred. New device programming algorithms will be necessary to make patient-customized programming in this lead configuration flexible, more useful clinically and easy.     

Correlates of reperfusion ventricular fibrillation in dogs

To elucidate determinants of reperfusion ventricular fibrillation (VF), regional myocardial blood flow, ATP, creatine phosphate (CP), heart rate and blood pressure were compared in 2 groups of anesthetized dogs: those that fibrillated spontaneously upon release of a 15-minute coronary artery occlusion (VF group, n = 8) and those that did not fibrillate when reperfused (No VF group, n = 27). Arterial pressure and heart rate before and during coronary artery occlusion were similar in both groups. Ischemie endo- and epicardial ATP values, measured at the end of the occlusion period, were reduced approximately 20% of nonischemic values in both groups. In contrast, CP (nmohmg protein^?1) within the ischemie zone was significantly lower in the VF group in both the epicardium (14.3 ± 1.6 in the VF group vs 22.8 ± 2.5 in the No VF group, p < 0.01) and the endocardium (9.0 ± 2.0 in the VF group vs 18.7 ± 1.8 in the No VF group, p < 0.01). Furthermore, epi- and endocardial regional myocardial blood flow in the center of the ischemic zone during occlusion was significantly lower in VF dogs than in No VF dogs. Epicardial flow was 0.06 ± 0.03 ml·min^?1·g^?1in VFdogsvs 0.44 ± 0.06 in No VF dogs (p < 0.001) and endocardial flow was 0.03 ± 0.02 ml·min^?1·g^?1 in VF dogs vs 0.23 ± 0.04 ·ml-min^?1·g^?1 in No VF dogs (p < 0.001). These data suggest that low levels of regional myocardial blood flow and CP during coronary artery occlusion are associated with an increased risk of VF on reperfusion. Thus, the severity of ischemia in the center of the ischemie zone may be a determinant of reperfusion VF.     

Selective right ventricular angiography in apparently idiopathic ventricular fibrillation

Summary The definition of underlying heart disease in apparently idiopathic ventricular fibrillation seems to be important in regard to prognosis and choice of therapy. From October 1989, until August 1993, cardiac arrest due to the documented ventricular fibrillation occurred in eight consecutive patients with normal results on clinical examination, normal echocardiography, and normal or apparently nonspecific electrocardiogram (ECG) findings. Complete invasive investigations, including selective right ventricular angiography, were done; regional hypokinesia and segmental bulging of the right ventricle were found in seven patients (88%). Arrhythmogenic right ventricular dysplasia was suspected in these patients, although endomyocardial biopsy was not performed. After the finding of localized right precordial QRS prolongation of more than 110 ms in November 1993 in five patients, a retrospective, a more precise approach to QRS duration in standard ECG supported this diagnosis. Selective right ventricular angiography is of great help in identifying underlying heart disease in patients with apparently idiopathic ventricular fibrillation, and confirms ECG findings.     

Prevention of ventricular fibrillation after aortic declamping during cardiac surgery

Ventricular fibrillation is common after aortic declamping during cardiac surgery, and the metabolic demands of such fibrillation, or its treatment by means of countershock, may contribute to myocardial injury. To determine the effects of administering intravenous lidocaine just before aortic declamping, we randomly divided 194 cardiac surgery patients into 2 groups. One hundred patients (group A) received lidocaine, 200 mg intravenously, 3 minutes before aortic declamping; and 94 patients (group B) received no medication before declamping. Multiple baseline variables, including clamp times, medications, electrolyte values, ventricular function, and the extent and type of surgery, were similar for both groups. After aortic declamping, 31 of the 100 patients in group A had ventricular fibrillation, as did 57 of the 94 patients in group B (p < 0.001). Of those who fibrillated, the group-A patients required a mean of 1.76 countershocks, whereas the group-B patients required a mean of 2.68 countershocks (p < 0.05). Serum potassium level also affected the incidence of ventricular fibrillation, independently of lidocaine. Elevated serum potassium levels were associated with a lower incidence of ventricular fibrillation. Although lidocaine was independently protective at all potassium levels, the combination of lidocaine and a high serum potassium level had the greatest effect in preventing fibrillation. In patients who had potassium levels higher than 5.1 mEq/l and who were also given lidocaine, the incidence of ventricular fibrillation was lower than 15%.     

Angiographic right and left ventricular function in arrhythmogenic right ventricular dysplasia

We prospectively documented right ventricular (RV) and left ventricular (LV) volumes and ejection fractions in a large series of patients with arrhythmogenic RV dysplasia/cardiomyopathy (ARVD/C). Eighty-five patients with ARVD/C and 11 controls underwent 2 successive orthogonal right and left monoplane x-ray-digitized cineangiographies. Volumes were calculated using the hemielliptical RV and ellipsoidal LV models. All controls and 58 of 85 patients (ARVD/C-I) had a RV ejection fraction > or =35% and 27 patients had a RV ejection fraction <35% (ARVD/C-II). Tricuspid annulus plane systolic excursion (TAPSE) was lower in ARVD/C-II than in ARVD/C-I patients (6 +/- 3 vs 14 +/- 3 mm) and controls (16 +/- 2 mm) (each p <0.001). In patients with ARVD/C, TAPSE was positively related to RV ejection fraction (r = 0.79) and to crista supraventricularis shortening (r = 0.81) (each p <0.001). Sensitivity and specificity of TAPSE <12 mm in identifying patients with RV ejection fraction <35% were 96% and 78%, respectively. LV ejection fraction was > or =50% in 68 patients, 40% to 49% in 10, and <40% in 7. Diffuse RV outflow tract aneurysm was observed in 9 patients, all belonging to ARVD/C-II, and this sign identified patients with LV ejection fraction <40% with 86% sensitivity and 96% specificity. In conclusion, 68% of ARVD/C patients had normal RV ejection fraction and RV volumes, and 80% of ARVD/C patients had normal LV ejection fraction. Decreased TAPSE <12 mm and a diffuse RV outflow tract aneurysm were sensitive and specific indicators of RV ejection fraction <35% and LV ejection fraction <40%, respectively.