Long-term follow-up of cardioverter-defibrillator implanted under conscious sedation in prepectoral subfascial position.

BACKGROUND: Implantable cardioverter-defibrillators (ICDs) with intravenous electrode systems and downsized generators can be implanted by use of operative techniques similar to those employed for the insertion of permanent pacemakers. However, the safety, efficacy, and long-term follow-up of simplified implantation procedures remain to be evaluated. This report is a prospective long-term evaluation of nonselected patients receiving ICDs in the prepectoral subfascial position under conscious sedation. METHODS AND RESULTS: Clinical characteristics of the 231 consecutive patients included a mean age of 63 years, a male-to-female ratio of 6.4, a left ventricular ejection fraction of 0.34, a mild-to-moderate heart failure in 91%, coronary artery disease in 84%, and a history of aborted sudden cardiac death or refractory ventricular tachyarrhythmias. Insertion of transvenous leads and prepectoral subfascial ICD implantation were performed in electrophysiology laboratories under local anesthesia and conscious sedation with intravenous midazolam and propofol. Successful implantation in all patients (operation time, 80 +/- 32 minutes, mean +/- SD) irrespective of body size and skin thickness was free of major complications, including need for emergency intubation. After surgery, 1 pocket hematoma, 1 seroma, and 1 pneumothorax required treatment. There was no operative or first-month mortality. During long-term follow-up averaging 453 +/- 296 days, six leads required repositioning, but pocket erosions or infections did not occur. First-year total survival was 97%. CONCLUSIONS: Implantation under conscious sedation of ICDs in the prepectoral subfascial position is a safe and effective procedure with low operative and postoperative morbidity and favorable long-term outcome.

Late follow-up of dual-chamber rate-adaptive pacing.

Dual-chamber pacing systems with sensor-based rate-adaptive capability (DDDR pacemakers) provide paced patients with the potential benefits of both a reliable chronotropic response and maintenance of atrioventricular (AV) synchrony. However, there is concern that clinical and programming complexities may necessitate frequent reprogramming of pacemakers from the DDDR mode to less physiologic pacing modes (in particular VVI or VVIR). Consequently, this study assessed the stability of pacing-mode programming, and the factors affecting pacing-mode selection in patients with a DDDR-capable pacing system. Clinical status during follow-up (18.2 +/- 6.7 months) was assessed in 75 patients. Principal diagnoses providing an indication for pacing were: (1) AV block alone, 18 of 75 patients (24%); (2) sick sinus syndrome alone, 41 (55%); and (3) combined AV block and sick sinus syndrome, 16 (21%). Twenty-three patients had history of atrial tachyarrhythmias. At implantation, 66 devices (88%) were programmed to DDDR mode, 7 (9%) to DDD, and 2 (3%) to DVIR. At last follow-up, the respective distribution of programmed modes was 83% DDDR, 10% DDD, 4% DVIR and 3% VVIR. During the study, the initial pacing mode remained unchanged in 54 patients (72%) and needed modification in 21 (28%). Of the latter 21 patients, atrial tachycardia was the basis for a programming change in 11 (52%), of whom 8 had history of atrial tachycardias. In general, postimplant atrial arrhythmia occurrences proved controllable, and ultimately return to a rate-adaptive dual-chamber pacing mode (DDDR, DDD or DVIR) was achieved in most cases. The remaining reprogrammings were primarily to optimize hemodynamic benefit.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of cycle length, cycle length alternans, and electrocardiographic lead in electrical alternans with rapid atrial pacing.

The role of cycle length and cycle length alternans in the induction of tachycardia-related QRS electrical alternans was investigated using an atrial pacing protocol in 16 patients. Pacing was performed at a cycle length less than 400 ms in 5 patients, greater than 400 ms in 5 and at both in 6 with 0, 6, 10, 20, 40 and 60 ms of atrial cycle length alternans. A 12-lead electrocardiogram and high right atrial, His bundle and right ventricular apical electrograms were simultaneously recorded after 30 to 60 seconds of pacing. Alternans was produced in 88% of patients. Alternans was 3 times more frequent at short (less than 400 ms) than long paced cycle lengths (greater than 400 ms) (66% vs 22%, p less than 0.0001). Alternans increased with increasing cycle length alternans and occurred with very little (less than or equal to 10 ms) atrioventricular nodal, His-Purkinje and ventricular cycle length alternans when paced cycle length was short. Alternans was more frequent in the precordial than the limb leads (45% vs 17%, p less than 0.001) and was most frequent in V3 and V2 (sensitivity 69% and 65%) and least frequent in leads I and aVL (sensitivity 4% and 10%). More leads per electrocardiogram showed alternans at short compared with long paced cycle lengths and the number of leads per electrocardiogram increased with increasing cycle length alternans. Occurrence of alternans was highly related to QRS amplitude by Spearman rank correlation (p less than 0.0005).(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of fascicular block on ventriculoatrial conduction during AV reentrant tachycardia.

Two patients with Wolff-Parkinson-White syndrome and surgically mapped anterior left free wall atrioventricular bypass tracts had orthodromic atrioventricular reentry tachycardia conducted with complete left bundle branch block (CLBBB), complete right bundle block (CRBBB), left anterior fascicular block (LAFB), and a narrow QRS. Ventriculoatrial conduction increased by 35 and 85 ms with CLBBB compatible with the left free wall location of the bypass tracts. In one patient, resolution of CLBBB occurred in two stages. Initially, left posterior fascicular block (LPFB) resolved, decreasing VA conduction by 20 ms. With resolution of the remaining LAFB, there was a further 15 ms decrease in VA conduction. In the other patient, the isolated occurrence of LAFB increased ventriculoatrial conduction by 30 ms. These changes confirmed the location of the bypass tracts in the anterior portion of the left ventricular free wall. Changes in VA conduction with fascicular block can help localize the ventricular insertion of atrioventricular bypass tracts.

Sudden death and its relation to QT-interval prolongation after acute myocardial infarction: two-year follow-up.

Risk of sudden death was assessed in 533 patients who survived 10 days after acute myocardial infarction (AMI) and were followed for up to 24 months (mean 18) in the Multicenter Investigation of the Limitation of Infarct Size. Analysis of clinical and laboratory variables measured before hospital discharge revealed that the QT interval, either corrected (QTc) or uncorrected for heart rate, did not contribute significantly to prediction of subsequent sudden death or total mortality. In this population, frequent ventricular premature complexes (more than 10 per hour) on ambulatory electrocardiographic monitoring and left ventricular (LV) dysfunction (radionuclide LV ejection fraction of 0.40 or less) identify patients at high risk of sudden death. In patients with these adverse clinical findings, the QTc was 0.468 +/- 0.044 second among those who died suddenly and 0.446 +/- 0.032 second in survivors, and was not statistically significant as an additional predictor of sudden death. Consideration of the use of type I antiarrhythmic agents, digoxin, presence of U waves and correction for intraventricular conduction delay did not alter these findings. Although QT-interval prolongation occurs in some patients after acute myocardial infarction, reduced LV ejection fraction and frequent ventricular premature complexes are the most important factors for predicting subsequent sudden death in this patient population.

Smoking-induced coronary vasoconstriction in patients with atherosclerotic coronary artery disease: evidence for adrenergically mediated alterations in coronary artery tone.

In patients with atherosclerotic coronary artery disease, cigarette smoking increases myocardial oxygen demand but may cause an inappropriate decrease in coronary blood flow and myocardial oxygen supply. This study was performed to explore the mechanism of smoking-induced coronary vasoconstriction and, specifically, to determine if smoking causes an alpha-adrenergically mediated increase in coronary artery tone. In 36 chronic smokers with coronary artery disease (27 men and nine women, 50 +/- 9 [mean +/- SD] years old), heart rate-systolic arterial pressure double product and coronary sinus blood flow (by thermodilution) were measured before and during smoking both before and after (1) normal saline (n = 5, control subjects), (2) an alpha-adrenergic-blocking agent, phentolamine, 5 mg (n = 15), (3) a beta-adrenergic-blocking agent, propranolol, 0.1 mg/kg (n = 12), or (4) sodium nitroprusside, 0.4 to 0.8 micrograms/kg/min, given in a dose sufficient to diminish systolic arterial pressure by 15% (n = 4). During the initial smoking period, rate-pressure product increased and coronary sinus blood flow was unchanged by smoking in all groups. After 30 to 75 min, saline, phentolamine, propranolol, or sodium nitroprusside was given, and measurements were repeated. In the control subjects, rate-pressure product and coronary sinus blood flow responded in a similar manner to that observed previously. In those receiving phentolamine, rate-pressure product was unchanged, but coronary sinus blood flow rose substantially with smoking (percent change +2 +/- 15% during the first smoking period [before phentolamine] and +32 +/- 17% during the second smoking period [after phentolamine]; p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Measurement of cardiac output without right heart catheterization: reliability, advantages, and limitations of a left-sided indicator dilution technique.

This study was done to determine the accuracy and reliability of cardiac output measurements by the injection of indocyanine green into the left ventricle, with simultaneous sampling from a systemic artery. In 40 patients (18 men, 22 women, aged 34 to 74 years), cardiac output was measured in close temporal proximity by (a) standard indicator dilution (right atrium-to-pulmonary artery thermodilution in 11, pulmonary artery-to-systemic artery indocyanine green in 29) and (b) left ventricle-to-systemic artery indocyanine green. There was excellent agreement between the two techniques (r = 0.98, SEE = 0.12 liters/minute). In 28 of the patients, cardiac output also was measured by ascending aorta-to-systemic artery indocyanine green. In these individuals, this technique yielded results that were disparate from those obtained by standard indicator dilution (difference between standard indicator dilution and left ventricle-to-systemic artery indocyanine green = 0.18 +/- 0.13 [mean +/- SD] liters/minute; difference between standard indicator dilution and ascending aorta-to-systemic artery indocyanine green = 0.72 +/- 0.55 liters/minute; p less than 0.001), and in 22 of the 28, the ascending aorta-to-systemic artery indocyanine green cardiac outputs were greater than those obtained by standard indicator dilution. Thus, cardiac output can be measured accurately by injecting indocyanine green into the left ventricle, with simultaneous sampling from a systemic artery, but it cannot be quantified reliably by introducing indicator into the ascending aorta. The left ventricle-to-systemic artery indocyanine green technique can be used in patients undergoing only left heart catheterization.(ABSTRACT TRUNCATED AT 250 WORDS)

Early positive technetium-99m stannous pyrophosphate images as a marker of reperfusion after thrombolytic therapy for acute myocardial infarction.

Fourteen patients with transmural acute myocardial infarction (AMI) were treated with intravenous streptokinase a mean of 4 +/- 1 hours after chest pain and underwent technetium-99m stannous pyrophosphate (Tc-99m-PPi) imaging 7 +/- 2 hours after the onset of chest pain. The early Tc-99m-PPi images were obtained to test the hypothesis that an early, strongly abnormal Tc-99m-PPi image suggests reperfusion. Eleven of 14 patients had early peaking (within 16 hours) serum creatine kinase isoenzyme levels (CK-B) at a mean of 11 +/- 3 hours. Ten of 14 patients had 3+ or 4+ acute Tc-99m-PPi images. Eight of 11 patients had patent infarct-related vessels at cardiac catheterization 15 days after AMI. One patient who had both an early positive Tc-99m-PPi image and CK-B peak level had an occluded infarct-related artery at catheterization. Acute left ventricular (LV) ejection fraction (EF) by radionuclide ventriculography was compared with LVEF on day 15, and improved from 0.37 +/- 0.13 to 0.50 +/- 0.16 (p = 0.004) in the 10 patients with strongly positive acute Tc-99m-PPi images. LVEF also improved from 0.37 +/- 0.12 to 0.49 +/- 0.15 (p = 0.003) in the 11 patients with early peaking serum CK-B values. Three patients without evidence of reperfusion failed to improve the LVEF from the initial value to the one obtained at hospital discharge. Six control patients had acute Tc-99m-PPi images 10 +/- 2 hours after chest pain; none had strongly positive acute Tc-99m-PPi images, and the mean time to peak CK-B was 19 +/- 5 hours.(ABSTRACT TRUNCATED AT 250 WORDS)