Effects of bradykinin on coronary blood flow and vasomotion in transplant patients.

OBJECTIVES: To evaluate the effects of exogenous bradykinin on coronary epicardial and microcirculatory tone in transplant patients (HTXs), and to compare them with the effects of acetylcholine. BACKGROUND: Coronary endothelial dysfunction has been reported to occur early after heart transplantation, most notably when acetylcholine was the endothelium-function marker used. The effects of bradykinin on coronary vasomotion are unknown in HTXs. METHODS: Sixteen HTXs were compared 3.6 +/- 1.7 months after transplantation to seven control subjects. Coronary flow velocity was measured using guide-wire Doppler. Diameters (D) of three segments of the left coronary artery and coronary blood flow (CBF) were assessed at baseline, after 3-min infusions of increasing bradykinin doses (50, 150 and 250 ng/min) then of increasing acetylcholine doses (estimated blood concentrations of 10(-8), 10(-7) and 10(-6) M). RESULTS: Bradykinin induced similar dose-dependent increases in D and CBF in both groups: D was 11 +/- 12%, 19 +/- 14% and 22 +/- 16% (all p < 0.0001), and CBF was 50 +/- 40%, 130 +/- 68% and 186 +/- 77% (all p < 0.0001). Acetylcholine induced significant epicardial vasodilation in control subjects and vasoconstriction in HTX, as well as a marked increase in CBF in both groups. Acute allograft rejection, present in 8 of the 16 HTXs, did not modify responses to bradykinin, but was associated with a smaller CBF increase in response to acetylcholine (p < 0.05). CONCLUSIONS: The coronary vasodilating effects of bradykinin are preserved early after heart transplantation, even in the presence of acute allograft rejection. Although there is an abnormal vasoconstricting response to acetylcholine reflecting endothelium dysfunction, the endothelium remains a functionally active organ in heart transplant recipients.

Coronary blood flow reserve and wall motion recovery in patients undergoing angioplasty for myocardial infarction.

AIMS: The aim of this study was to evaluate the relationship between coronary flow reserve and the recovery of wall motion contractility in patients with recent myocardial infarction. METHODS AND RESULTS: Nineteen patients (55 +/- 8 years) undergoing balloon angioplasty for recent myocardial infarction were studied. After angioplasty, coronary flow reserve was lower in the infarct-related artery than in a reference artery, 2.2 +/- 0.6 and 2.8 +/- 0.7, respectively, P < 0.05. There was no immediate correlation between coronary blood flow reserve measured after angioplasty and wall motion index. There was a negative correlation between coronary flow reserve and the number of necrotic segments (r = -0.43; P0.006). At the 4 month control angiogram, there was a significant increase in both left ventricular ejection fraction (59 +/- 14% vs 51 +/- 13%; P < 0.05) and wall motion index (-0.63 +/- 1.2 vs -1.94 +/- 0.9 units SD, P = 0.005). In patients in whom wall motion improved (> 1 unit SD), the immediate coronary flow reserve was higher (P < 0.05) than in patients without improved wall motion. In this group, the increase in wall motion index was correlated to the coronary blood flow reserve (r = 0.55; P < 0.02). CONCLUSION: These data show that after myocardial infarction, coronary flow reserve is associated with myocardial viability.

Long-term performance of endocardial pacing leads.

To assess the performance of endocardial pacemaker leads and to identify factors associated with structural lead failure, medical records of 2,611 endocardial pacing leads (in 1,518 patients) implanted between 1980 and 1991, having at least 1 month of follow-up, were reviewed. Leads without structural failure had normal function at the last follow-up date, or were discontinued for reasons other than structural failure (patient death, infection, dislodgment, lead-pacemaker incompatibility, operative complication, or abandonment by telemetry not related to failure). Leads with suspected structural failures were invasively or noninvasively disconnected because of clinical malfunction (loss of capture or sensing, oversensing, elevated thresholds, or skeletal muscular stimulation). Leads with verified structural failures met the criteria for suspected lead failure and also had a visible defect seen in the operating room or on chest roentgenograms, a change in the impedance interpreted by the physician as lead disruption, or a manufacturer's return product report that confirmed structural failure. Variables analyzed included patients' age and gender, paced chamber, venous access, insulation materials, fixation mechanism, coaxial design, polarity, and different lead models. The cumulative lead survival at 5 and 10 years were 97.4% and 92.9%, respectively, for suspected failures; and 98.7% and 97.3%, respectively, for verified failures. Leads in older patients (> or = 65 years old), and leads in atrial position had fewer verified failures (P = 0.014 and P = 0.007, respectively). Unipolar leads also tended to perform better according to the verified definition (P = 0.07).(ABSTRACT TRUNCATED AT 250 WORDS)

Durability of bipolar coaxial endocardial pacemaker leads compared with unipolar leads.

BACKGROUND: The coaxial design allows for thinner bipolar endocardial pacemaker leads, but recent reports have suggested a higher incidence of failure for this sophisticated configuration. OBJECTIVE: To compare the long-term survival of bipolar coaxial and unipolar leads. METHODS: Retrospective follow-up. RESULTS: Between January 1, 1980 and June 30, 1991, 1142 bipolar coaxial leads and 1181 unipolar leads were implanted at the Cleveland Clinic. The mean follow-up was 33 +/- 32 months (range 1 to 138 months). Ten bipolar coaxial leads failed (0.88%), as did 9 unipolar leads (0.76%). At 5 years the cumulative survival was 98.6% for both types of leads; however, at 10 years the survival of bipolar coaxial leads was only 92.4% compared with 98.6% of unipolar leads (P = .03; relative risk 2.7, 95% confidence interval = 1.1 to 6.9). CONCLUSIONS: The sophisticated design of bipolar coaxial leads could be the cause of their increased vulnerability. The benefit-to-risk ratio of this design should be prospectively reevaluated.

Long-term performance of epimyocardial pacing leads in adults: comparison with endocardial leads.

The long-term performance of epimyocardial pacing leads in children is well established, but few studies have analyzed the performance in adults. This issue has clinical relevance in view of the increased use of epimyocardial leads with implantable cardioverter defibrillator and antitachycardia pacing systems. We analyzed 93 epimyocardial pacing "systems" (121 leads: 65 unipolar, 28 bipolar) in adult patients (age 57 +/- 16 years), implanted since January 1980. Two different models were studied: Medtronic 4951 "Stab-on" (n = 35) and Medtronic 6917/6917A "Screw-in" (n = 58). A control group was created by randomly matching each epimyocardial system with two endocardial leads, according to age and year of implant. Epimyocardial and endocardial leads were followed-up for 44 +/- 35 and 43 +/- 35 months, respectively (P = NS). Freedom from failure for epimyocardial leads was 0.91 (95% Confidence Interval [95% CI] = 0.82 to 0.96) at 5 years, and 0.91 (95% CI = 0.69 to 0.98) at 10 years. No difference was found between the two analyzed models. Freedom from failure for endocardial leads was 0.97 (95% CI = 0.93 to 0.99) and 0.90 (95% CI = 0.61 to 0.97) at 5 and 10 years, respectively. Epimyocardial leads had a significantly poorer short-term survival than endocardial leads, secondarily to earlier "technique related" failures (P = 0.03; relative risk 3.0; Wilcoxon test). However, overall long-term performance was similar to endocardial leads. Epimyocardial pacing leads, meticulously implanted and tested, have a long-term performance similar to endocardial pacing leads.

Pacing lead survival: performance of different models.

UNLABELLED: Recent reports have shown poor survival of some leads currently in use. Long-term survival analysis of 2,444 leads (1,059 atrial and 1,385 ventricular) implanted in this institution since January 1980, and having at least 1 month of follow-up was performed. The survival of 123 different models was compared with the average survival of all the leads implanted in the corresponding chamber. Failure was defined as inactivation of the lead (electrical abandonment, explant, or cap) due to insulator and/or conductor fracture. RESULTS: The mean follow-up was 33 +/- 32 months. The cumulative survival for different atrial lead models was consistent with the average performance in the atrium. No atrial lead showed better or worse survival compared to the others. In the ventricular group, the Medtronic 4012 lead showed statistically significant poorer survival (P = 0.01) compared with the average survival of the ventricular leads. The Cardiac Pacemakers, Inc. (CPI) 4010 lead showed a nonsignificant (P = 0.12) worse performance than the average for ventricular leads. CONCLUSIONS: (1) The Medtronic 4012 had a significantly poorer performance than the rest of the leads. A trend in similar direction was found for the CPI 4010, also in the ventricular group; (2) Atrial lead models showed a stable survival; and (3) Frequent follow-up is required for some leads, especially in pacemaker dependent patients.

Physiology of rate-responsive pacing.

The search for a pacemaker that accurately and easily mimics normal physiology is a continuing effort. There have been many achievements in the past, including sensing of the pacing chamber and programming of the pacing rate, sensitivity, and output. Present pacing developments include atrioventricular synchrony and rate adaptiveness. Results of studies on activation sequence and circadian variations will impact future pacing. The usefulness, cost effectiveness, and clinical value of some of the new pacing features remain unclear. Further clinical trials are necessary to clarify the value of new pacing techniques.