Lack of Physiological Adaptation of the Atrioventricular Interval to Heart Rate in Patients Chronically Paced in the AAIR Mode

Seventeen consecutive patients, aged 56 +/- 12, were chronically paced in the AAIR mode for a symptomatic sinus node disease with atrial chronotropic incompetence defined by a peak exercise heart rate (HR) less than 75% of the maximal predicted heart rate (MPHR) mean = 65 +/- 10%). Sensors used were activity sensing (n = 7), minute ventilation (n = 6), or respiratory rate (n = 4). Basic pacing rate was programmed at 71 +/- 5 beats/min and the maximal sensor rate at approximately 85% MPHR (143 +/- 10); other sensor parameters were programmed individually. Six months after implant, two standardized and symptom limited exercise tests were performed in random order, AAI and AAIR modes, respectively. AAIR pacing significantly improved peak exercise HR (139 +/- 14 vs 112 +/- 30 beats/min; P less than 0.01), maximal sustained workload (132 +/- 42 vs 110 +/- 38 watts; P less than 0.02), and total exercise duration (724 +/- 299 vs 594 +/- 245 sec; p less than 0.02) compared to the AAI mode. In all 17 patients, HR was continuously sensor driven in the AAIR mode, making it possible to precisely study the adaptation of the stimulus-R interval and of the stimulus-R:RR ratio during exercise. Six patients normally adapted with a progressive shortening. Six others did not adapt at all without any variation of interval. Five patients paradoxically increased their stimulus-R interval (286 +/- 10 msec at peak E vs 220 +/- 19 msec at rest) and their stimulus-R:RR ratio (67 +/- 20% vs 29 +/- 4%), producing P waves occurring immediately after, or even within the R wave of the preceding cycle; two patients complained of severe exercise related symptoms corresponding to the so-called "AAIR pacemaker syndrome." The principal factors involved in the nonadaptation of AV interval to HR were related to the patient (organic heart disease, with the particular problem of the denervated heart; the bradytachy syndrome; and the use of drugs, especially beta blockers and Class I antiarrhythmic drugs) or to the pacemaker ("overstimulation" phenomenon). These observations constitute an additional argument for wider indications of implanting DDDR units in these patients.     

Percutaneous Mechanical Mitral Commissurotomy with the Metallic Valvulotome: Detailed Technical Aspects and Overview of the Results of the Multicenter Registry on 882 Patients

Percutaneous mechanical mitral commissurotomy (PMMC) is a new technique that has been developed over the last 3 years for the treatment of mitral stenosis. The device used opens the commissures by a direct action of two parallel bars located in a metallic head screwed at the distal end of a 13Fr catheter. Opening of the bars is obtained with the use of activating pliers attached at the proximal end of the catheter. The metallic dilator and the pliers can be safely reused after sterilization. The device and the direrent steps of the procedure are detailed in this article. The results of an international registry including 882 patients are reported here. PMMC could be achieved in 863 (98%) cases. Maximal opening of the bars was 40 mm in 90% of the cases. The technique resulted in an increase of the mitral valve area from 0.94 ± 0.2 cm² to 2.12 ± 0.4 cm². Bilateral splitting of the commissures was achieved in 85% of the cases. Complications occurred in 33 (3.7%) patients: pericardial tamponade in 1.4% (12 cases, one death), mitral regurgitation > grade 2 in 2.1% (18 cases, surgery required in 4), and transient stroke in 0.3% (3 patients). The role of the learning curve in the occurrence of complications has been clearly demonstrated. The cost of the procedure has been markedly decreased in developing countries due to multiple reuses of the device after sterilization.     

Immediate effects of captopril in acute left ventricular failure secondary to myocardial infarction

Abstract. In eight patients with acute left ventricular failure secondary to myocardial infarction the haemo-dynamic effects of captopril (25 mg), an orally active converting enzyme inhibitor, were measured. Haemo-dynamic modifications were maximal at 60 min and lasted for 2–3 h. Pulmonary wedge pressure fell from 23–5± 4.9(mean ± SD)to 16–8 ± 4.7 mmHg(P<0–01), cardiac output rose from 3–24 ± 1 to 4–05 ± 0–91 1/min (P<001). Systemic vascular resistance decreased from 27–34 ± 3–81 to 17.52 ± 1–65 mmHg min 1^-1 (P<001). Mean arterial pressure fell from 89.6 ± 13.9 to 75.7±0 16.3 mmHg (P<0001) while heart rate was not significantly modified. Six patients who had high pretreatment plasma renin activity values responded by a decrease in ventricular filling pressure and/or an increase in cardiac output. One patient with normal initial plasma renin activity value showed similar haemodynamic effects. These data suggest that in the short term captopril is a vasodilator with both arterial and venous effects and improves cardiac function in acute left ventricular failure secondary to myocardial infarction.