Long-term assessment of unipolar and bipolar stimulation and sensing thresholds using a lead configuration programmable pacemaker.

Acute and long-term pacing thresholds were measured prospectively in 74 patients with a unipolar/bipolar multiprogrammable pacemaker. At implantation, mean current threshold was 0.48 +/- 0.16 mA with unipolar mode and 0.55 +/- 0.16 mA bipolar mode (p less than 0.01). R wave amplitude at implantation was 7.78 +/- 2.4 mV with unipolar and 7.67 +/- 2.1 mV in bipolar mode (p = NS). During long-term follow-up (mean 9.3 months; range 3 to 24), no clinically significant differences in pacing or sensing thresholds were observed between bipolar and unipolar configurations. Lead configuration was changed 23 times in 11 patients. Symptomatic myopotential inhibition was corrected in two patients by reprogramming to the bipolar pacing mode. High thresholds and loss of capture were corrected in two patients by reprogramming to the unipolar pacing mode. The remaining configurational changes were made for improved sensing or pacing thresholds. This study documents, in a large group of patients, the equivalence of long-term unipolar and bipolar pacing and sensing thresholds and, in addition, demonstrates that lead configuration programmability offered some advantage in a subgroup of patients and may have prevented reoperation in five patients.

Clinical significance of perfusion defects by thallium-201 single photon emission tomography following oral dipyridamole early after coronary angioplasty.

The clinical significance of myocardial perfusion defects present early after angiographically successful percutaneous transluminal coronary angioplasty was assessed in 53 patients using thallium-201 single photon emission computed tomography combined with pharmacologic vasodilation induced by a large dose (300 mg) of orally administered dipyridamole. Myocardial tomographic images were obtained at a mean of 20 +/- 6 h (SD) before and 2.9 +/- 2.7 days after angioplasty. Before angioplasty, 15 (28%) of the 53 patients developed angina after dipyridamole administration, in contrast to only 3 (7.5%) of 40 patients after angioplasty (p less than 0.001). The mean percent luminal area stenosis decreased from 93 +/- 6% before angioplasty to 34 +/- 17% after angioplasty (p less than 0.001). Myocardial perfusion defects, present in 49 (93%) of the 53 patients before angioplasty, were reversible in 44 patients (83%), all of whom underwent dilation of arteries supplying the ischemic areas. After angioplasty, 26 (65%) of 40 patients had no ischemic defects, whereas 14 (35%) of the patients still had an ischemic defect in the vascular territory of the dilated artery. After a mean follow-up period of 21.7 months, 13 (33%) of 39 patients developed restenosis, 10 of whom had an ischemic defect early after angioplasty. Restenosis developed in 10 (71%) of 14 patients with an ischemic defect after angioplasty, but in only 3 (11.5%) of the patients without an ischemic defect (p = 0.007). In conclusion, thallium-201 tomography after oral dipyridamole affords convenient assessment of the physiologic significance of coronary stenosis present before angioplasty and the residual stenosis after angioplasty.(ABSTRACT TRUNCATED AT 250 WORDS)

Intracoronary thrombolytic therapy in acute myocardial infarction: a prospective, randomized, controlled trial.

A prospective, randomized trial was designed to assess the efficacy of intracoronary thrombolytic therapy with streptokinase (STK) in acute myocardial infarction. Sixty-four patients with acute myocardial infarction were randomized within 6 hours of onset of symptoms to 1 of 3 groups. Sixteen patients were treated by conventional means (control group). Nineteen patients underwent coronary arteriography and received corticosteroids and intracoronary and intravenous nitroglycerin (NTG group). Twenty-nine patients received management identical to that of the NTG group, with the addition of intracoronary STK therapy (STK group). Recanalization was demonstrated in 21 of 29 patients (72%) in the STK group. Global and regional ejection fraction (EF) was determined by radionuclide ventriculography before any intervention and 7 to 10 days later. No significant improvement in global EF was achieved in the control and NTG groups. In STK patients as a group, global EF did not increase significantly; however, in patients recanalized with STK, EF improved from 42 +/- 17% to 49 +/- 16% (p = 0.023). All groups showed wide variability of response. Improvement in global EF of more than 5% was noted in 44% of patients recanalized with STK. When subgrouped on the basis of initial global EF of 45% or less or more than 45%, only patients recanalized with STK with an initial EF of 45% or less had an improved global EF (from 30 +/- 10% to 42 +/- 10%, p = 0.015).(ABSTRACT TRUNCATED AT 250 WORDS)

Malposition of transvenous pacing lead in the left ventricle.

Transvenous pacemaker lead malposition in the left ventricle occurs rarely and requires a high index of suspicion for proper diagnosis. The case of a woman with unintentional lead placement in the left ventricle is presented. She had two episodes of transient neurologic deficits, possible secondary to embolic events, and was started on oral anticoagulants. Chest x-ray and electrocardiogram (ECG) suggested pacemaker lead malposition and transesophageal echocardiography revealed sinus venosus atrial septal defect. The lead was shown to cross the atrial septum and the mitral valve to the left ventricle. The malpositioned lead was successfully removed from the left ventricle at the time of surgical repair of the atrial septal defect. The potential value of 12-lead ECG, chest x-ray, posteroanterior and lateral views, and echocardiography in the diagnosis of pacemaker lead malposition are discussed and recommendations to avoid this complication at the time of pacemaker implant are outlined.

Quantification of infarct size by 201Tl single-photon emission computed tomography during acute myocardial infarction in humans. Comparison with enzymatic estimates.

We prospectively investigated whether 201Tl single-photon emission computed tomography (SPECT) could accurately diagnose the presence and quantify the extent of acute myocardial infarction when compared with infarct size assessed by plasma MB-creatine kinase activity. Thirty patients with enzymatic evidence of infarction were imaged within 12-36 hours of chest pain (mean, 23.4 hours). No patient had a previous infarction, and none underwent intervention seeking to restore coronary patency. Infarct size was quantified with computer-generated polar maps of the myocardial radioactivity and expressed as a percentage of the total left ventricular volume. To assess left and right ventricular performance, blood-pool gated radionuclide angiography was performed immediately after SPECT. All 30 patients had perfusion defects consistent with myocardial infarction. Scintigraphic and enzymatic estimates of infarct size correlated well for the group as a whole (r = 0.78, p less than 0.001, SEE = 9.1) but especially for those patients with anterior infarction (r = 0.91, p less than 0.001, SEE = 7.9). The poor correlation observed in patients with inferior infarction (r = 0.50, p less than 0.05, SEE = 10.0) was believed to be related to the frequent occurrence of right ventricular involvement because SPECT assessed only left ventricular damage, whereas the enzymatic method estimated the myocardial injury in both ventricles. A quantitative index of right ventricular infarct size, derived from the relation between the scintigraphic and enzymatic estimates, had a strong inverse correlation with right ventricular ejection fraction (r = -0.89, p less than 0.001, SEE = 3.6).(ABSTRACT TRUNCATED AT 250 WORDS)