Clinical experience with steroid-eluting unipolar electrodes.

In continuing search of low chronic threshold leads, a new concept of electrode design which is capable of delivering corticosteroids at the myocardial tissue interface has been made available by Medtronic. Twenty-three patients, 17 females and 6 males, were either implanted with 4003 (n = 21) or 5023 (n = 2) steroid-eluting electrodes in the ventricular chamber. Pacing modes utilized were VVIM (n = 13) or DDD (n = 10). Pulse generators used were Medtronic (7005, 8317, 8329) Pacesetter (285) and Intermedics (283). Thresholds at the time of implantation at 0.50 msec pulse width were 0.40 +/- 0.02 volts at 0.66 +/- 0.05 milliamps. Resistance and R wave measured were 565.43 +/- 22.07 ohms and 9.24 +/- 1.06 mv, respectively. Chronic thresholds were checked on routine follow-up visits by either decreasing pulse width and/or pulse amplitude. Data is being reported between 1 and 88 (23.22 +/- 4.35) weeks. Pulse width threshold at 2.5 volts were 0.10 msec (n = 11) and 0.05 msec or lower (n = 12). At 5.0 volts no loss of capture was seen at 0.05 msec (n = 22) except in one patient at 0.10 msec. Pulse width thresholds in the first 24 weeks were lower than 0.20 msec at 2.5 volts (n = 15) and less than 0.70 msec. at 0.8 volts (n = 6). No loss of sensing was seen by electrocardiographic analysis at the time of threshold checks with the pulse generator at standard setting of the R wave. Thus, in this initial report, the steroid-eluting electrodes have demonstrated very low thresholds both in the early and chronic follow-up phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Five-year performance of the Medtronic 6971 polyurethane endocardial electrode.

There is a considerable debate over the long-term performance of polyurethane electrodes. Observation to date has demonstrated surface cracking and some clinical failures in patients. Since 1978 we have implanted about 82 6971 Unipolar Medtronic electrodes in the ventricle. In 33 patients, lead integrity was assessed by chronic thresholds determined by decreasing pulse width and pulse amplitude. Sensing functions were assessed by electrocardiographic rhythm analysis. At a follow-up between 7 and 67 months, chronic thresholds at 2.50 volts were 0.08 +/- 0.04 milliseconds in 26 patients with Medtronic Pulse generators (Models 8423, 5985, and 7000). In two patients with similar units, no loss of capture was seen even at 0.05 milliseconds. Three patients, one with Cordis Unit (233F) showed loss of capture at 0.20 milliseconds at 2.00 MA, the other with a Pacesetter unit (255-6) showed loss of capture at 0.20 milliseconds, at 2.50 volts. One patient with Intermedics unit (283) lost capture at 0.07 milliseconds at 2.70 volts. Insulation breaks seen in two patients were demonstrated by pectoral stimulation and pacemaker oversensing. In addition, 24-hour long-term electrocardiographic monitoring was performed in 22 patients between 23 to 70 months. Appropriate pacemaker function was seen except in one patient who demonstrated oversensing. Interruption in insulation was demonstrated at the ligature site at exploration. Thus, in this series of patients who were paced in the ventricle by the 6971 Medtronic electrode, only two patients have demonstrated insulation failure. The incidence of insulation break in this polyurethane unipolar electrode is uncommon and occurs at further stress points.

Experimental myocardial infarction. 14. Accelerated myocardial stiffening related to coronary reperfusion following ischemia.

In six dogs with surgically opened chests, segmental mechanical function was determined by measuring segment length using mercury-in-Silastic gauges attached to the epicardial surface of the left ventricular wall. Following coronary arterial occlusion the amplitude of the resulting paradoxical systolic bulge was quantitated in terms of "muscle lengths", defined as the ratio of the amplitude of the segment length over the end-diastolic segment length (EDSL). From an excursion of 0.176 +/- 0.029 muscle lengths at six hours of ischemia, the amplitude of the bulge decreased abruptly to 0.125 +/- 0.024 muscle lengths after 15 minutes of coronary reperfusion (P less than 0.05) but maintained paradoxical expansion in systole. Segmental "effective stiffness", calculated at the same periods of time from end-diastolic pressure-length relationships during transient pressure loading of the left ventricle, showed a reciprocal change, increasing from 1.416 +/- 0.161 to 2.051 +/- 0.238 mm Hg/% deltaEDSL (P less than 0.05). These data indicate that the degree of paradoxical bulging of an ischemic segment is affected by its pressure-length characteristics (distensibility) and that a rapid decrease both in the amplitude of the bulge and in distensibility occurs during reperfusion. The mechanism is uncertain but may relate to either myocardial edema or myofibrillar contracture.

Persistence of myocardial injury following brief periods of coronary occlusion.

Transient (20 min) occlusion of the left anterior descending coronary artery in open-chest anaesthetized dogs caused immediate aneurysmal bulging of the ischaemic segment, which preceded epicardial ST-segment elevation. Reperfusion after 20 min restored epicardial electrograms to normal, wheras mechanical dysfunction persisted for a least 45 min therafter. The study shows that there is temporal disparity between electrical and mechanical events both at the inception of myocardial ischaemia and during recovery from transient myocardial ischaemia.

Experimental myocardial infarction. XIII. Sequential changes in left ventricular pressure-length relationships in the acute phase.

Diastolic pressure-length relationships of an ischemic region of the canine left ventricle were measured over a six-hour period following left anterior descending coronary artery ligation, and their evolution was compared with the extent of systolic aneurysmal bulging. Normalized ischemic segment length excursion, which after coronary artery ligation may be taken as a measure of systolic aneurysmal bulging, increased during the first hour after ligation but thereafter declined toward control values. Concurrently, reciprocal changes were demonstrated in the slope of the end-diastolic pressure-length curves obtained during transient pressure loading of the left ventricle. These data show that the magnitude of acute systolic aneurysmal bulging followed experimental coronary artery ligation is determined not only by loss of contractile function, but also by changes in passive pressure-length relationships of the myocardium. Moreover, the results indicate that development of akinesis in experimental ischemia, heretofore demonstrated only in the chronic phase of infarction, may begin within hours of the onset of myocardial ischemia.

Effects of hypoxia, cyanide, and ischaemia on myocardial contraction: observations in isolated muscle and intact heart.

Using potassium cyanide (KCN) to stimulate hypoxia, the effects of intracoronary injections of KCN were compared with total occlusions of the same vessel. Imparied contraction as measured by segment length gauges was of equally abrupt onset following both interventions. The magnitude of systolic expansion at one minute was more marked following total occlusion than after KCN administration.