Differential effects of atropine and isoproterenol on inducibility of atrioventricular nodal reentrant tachycardia.

BACKGROUND: Radiofrequency ablation of the "slow pathway" in atrioventricular nodal reentrant tachycardia (AVNRT) relies on tachycardia non-inducibility after ablation as success criterion. However, AVNRT is frequently non-inducible at baseline. Thus, autonomic enhancement using either atropine or isoproterenol is frequently used for arrhythmia induction before ablation. METHODS: 80 patients (57 women, 23 men, age 50+/-14 years) undergoing slow pathway ablation for recurrent AVNRT were randomized to receive either 0.01 mg/kg atropine or 0.5-1.0 microg/kg/min isoproterenol before ablation after baseline assessment of AV conduction. The effects of either drug on ante- and retrograde conduction was assessed by measuring sinus cycle length, PR and AH interval, antegrade and retrograde Wenckebach cycle length (WBCL), antegrade effective refractory period (ERP) of slow and fast pathway and maximal stimulus-to-H interval during slow and fast pathway conduction. RESULTS: Inducibility of AVNRT at baseline was not different between patients randomized to atropine (73%) and isoproterenol (58%) but was reduced after atropine (45%) compared to isoproterenol (93%, P<0.001). Of the 28 patients non-inducible at baseline isoproterenol rendered AVNRT inducible in 21, atropine in 4 patients. Dual AV nodal pathway physiology was present in 88% before and 50% after atropine compared to 83% before and 73% after isoproterenol. Whereas both drugs exerted similar effects on ante- and retrograde fast pathway conduction maximal SH interval during slow pathway conduction was significantly shorter after isoproterenol (300+/-48 ms vs. 374+/-113 ms, P=0.012). CONCLUSION: Isoproterenol yields higher AVNRT inducibility than atropine in patients non-inducible at baseline. This may be caused by a more pronounced effect on antegrade slow pathway conduction.

Myocardial viability assessment by endocardial electroanatomic mapping: comparison with metabolic imaging and functional recovery after coronary revascularization.

OBJECTIVES: The objective of this study was to compare electroanatomic mapping for the assessment of myocardial viability with nuclear metabolic imaging using positron emission computed tomography (PET) and with data on functional recovery after successful myocardial revascularization. BACKGROUND: Animal experiments and first clinical studies suggested that electroanatomic endocardial mapping identifies the presence and absence of myocardial viability. METHODS: Forty-six patients with prior (> or =2 weeks) myocardial infarction underwent fluorine-18 fluorodeoxyglucose (FDG) PET and Tc-99m sestamibi single-photon emission computed tomography (SPECT) before mapping and percutaneous coronary revascularization. The left ventricular endocardium was mapped and divided into 12 regions, which were assigned to corresponding nuclear regions. Functional recovery using the centerline method was assessed in 25 patients with a follow-up angiography. RESULTS: Regional unipolar electrogram amplitude was 11.0 mV +/- 3.6 mV in regions with normal perfusion, 9.0 mV +/- 2.8 mV in regions with reduced perfusion and preserved FDG-uptake and 6.5 mV +/- 2.6 mV in scar regions (p < 0.001 for all comparisons). At a threshold amplitude of 7.5 mV, the sensitivity and specificity for detecting viable (by PET/SPECT) myocardium were 77% and 75%, respectively. In infarct areas with electrogram amplitudes >7.5 mV, improvement of regional wall motion (RWM) from -2.4 SD/chord +/- 1.0 SD/chord to -1.5 SD/chord +/- 1.1 SD/chord (p < 0.01) was observed, whereas, in infarct areas with amplitudes <7.5 mV, RWM remained unchanged at follow-up (-2.3 SD/chord +/- 0.7 SD/chord to -2.4 SD/chord +/- 0.7 SD/chord). CONCLUSIONS: These data suggest that the regional unipolar electrogram amplitude is a marker for myocardial viability and that electroanatomic mapping can be used for viability assessment in the catheterization laboratory.

Effects of blood pressure reduction on the elastic profile of the aortic tree in patients with coronary heart disease.

Decreased arterial compliance of large arteries in coronary heart disease has been reported. Using intravascular ultrasound it was demonstrated that arterial compliance decreases with increasing distance from the heart. Until now changes in the elastic profile have not been investigated after a stepwise blood pressure (BP) reduction induced by antihypertensive agents. The local viscoelastic properties of the aortic tree were analyzed before and after a mean arterial BP reduction of about 5 and 15 mm Hg below baseline by the steady-state infusion of increasing doses of nisoldipine in 15 patients with coronary artery disease. Intravascular ultrasound imaging combined with arterial pressure measurements were performed at five sites along the aortic tree to determine the viscoelastic profile before nisoldipine administration and again after the 5 and 15 mm Hg nisoldipine-induced blood pressure reductions. The elasticity parameters varied depending on the distance from the heart and on the BP level. At both BP reduction levels nisoldipine infusion led to an increase in arterial compliance at the abdominal aorta and at the aortic bifurcation. A dissociation between the 5 and the 15 mm Hg BP reduction was found at the common iliac artery and at the external iliac artery. Our results provide direct quantitative evidence that stepwise BP reductions exhibit different and, in part, contrary effects on the elastic profile, depending on the aortic tree location. The results also suggest that nisoldipine infusion can significantly ameliorate local viscoelastic properties at the abdominal aorta and at the aortic bifurcation, an effect that was associated or caused by a change in BP attributable to a decrease in peripheral resistance.

[Do heart transplant patients benefit from rate-adjusted electrostimulation?]. / Profitieren herztransplantierte Patienten von einer frequenzadaptierenden Elektrostimulation?

Exercise capacity of heart transplant recipients is limited in comparison to normals and, due to cardiac denervation, exercise-induced heart-rate response is blunted in these patients. In order to evaluate the effect of rate-responsive atrial pacing on exercise capacity, 13 patients (three female, 10 male; age: 53 +/- 7 years) were studied 2-35 months after orthotopic heart transplantation. Spiroergometry with breath-to-breath gas analysis was performed during a progressive supine bicycle test with a starting workload of 25 watts and increments of 15 watts every minute. In comparison to 10 normals (two female, eight male; age: 51 +/- 7 years) maximal heart rate (127 +/- 17 vs. 146 +/- 12 min-1), maximal work load (107 +/- 27 vs. 208 +/- 42 watts) and oxygen consumption at the anaerobic threshold (9 +/- 2 vs. 18 +/- 4 ml/kg/min) were significantly reduced in heart transplant recipients (p < 0.05). During the exercise test the p-waves of the remaining part of the recipients' atria were registered via a transoesophageal catheter. The maximal rate of the innervated recipients sinus node (146 +/- 15 min-1) was equal to the maximal heart rate of the control group. The exercise protocol was repeated during atrial stimulation of the transplanted hearts. To achieve a physiological adaptation of the heart rate, the pacing rates were adjusted to the rates of the recipients sinus node. In comparison to the previous tests an improvement of cardiopulmonary exercise capacity was not observed during rate adaptive pacing.

Successful treatment of massive pulmonary embolism by combined mechanical and thrombolytic therapy.

In two patients with massive pulmonary embolism and cardiogenic shock requiring mechanical ventilation and prolonged external cardiac massage, occluded pulmonary arteries were recanalized by primary mechanical fragmentation of thrombi using a percutaneously inserted catheter followed by fibrinolytic therapy. The hemodynamic and respiratory parameters rapidly and greatly improved. Pulmonary angiography before discharge revealed normal results in both patients. No central neurological abnormalities were detected. It is concluded that patients with cardiogenic shock due to massive pulmonary embolism may benefit from immediate mechanical thrombus fragmentation followed by fibrinolysis when thrombolysis or surgical embolectomy are strictly contraindicated or not available.