Clinical experience with the implantable cardioverter-defibrillator.
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Biomedical subjects
Publications and source records attributed to L S Griffith.
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A set of electrocardiographic criteria for the diagnosis of coronary artery disease was evaluated in two different groups of patients examined by computer aided 12 lead exercise electrocardiographic stress testing and coronary arteriography. One group consisted of patients with severe angina pectoris and the other of patients who had suffered a myocardial infarction three years before the study. Angiographically determined categories of patients could be identified with satisfactory precision by the electrocardiographic criteria under test in the patients with angina pectoris but not in those with infarction. A new method of classifying patients on the basis of data from coronary arteriography improved the correlation with ST segment analysis compared with conventional classification.
Since February, 1980 nearly 200 automatic cardioverter - defibrillators have been implanted in patients with malignant ventricular arrhythmias. The currently-employed device weighs 298 grams and occupies a volume of 162 cm3. There are two defibrillation electrodes which also serve as sensors: one, an intravascular catheter placed in the superior vena cava at the level of the right atrium; the other, a flexible rectangular patch placed extrapericardially over the apex of the heart. Additionally, there is a bipolar right ventricular electrode for rate counting and R-wave synchronization which will eventually be used for pacing as well. The unit is powered by lithium batteries with a projected monitoring life of three years, or the capability of discharging approximately 100 times. The arrhythmia detector activates the cardioverter -defibrillator about 15 to 20 seconds after diagnosing a "treatable" arrhythmia, identified on the basis of a striking absence of isoelectric potential segments characteristic of ventricular fibrillation and many ventricular tachycardias. The diagnosis also requires fulfillment of individually-programmed heart rate criteria. If the initial discharge of 25 joules is ineffective, the device will recycle as many as three times with a final pulse of up to 42 joules. Of the twelve nonsurvivors among the initial 52 implantees who underwent implantation through September, 1982, only four deaths were unwitnessed and considered to be sudden and arrhythmic; the other eight deaths were due to heart failure or unrelated causes. Thus, from a predicted mortality of 48% in the same group of patients if the automatic defibrillator had not been implanted, the "sudden death" mortality was reduced to 8.5%.
An R-wave synchronous implantable automatic cardioverter-defibrillator (IACD) was evaluated in 12 patients with repeated episodes of cardiac arrest who remained refractory to medical and surgical therapy. Seven men and 5 women, average age 61 years, surgically received a complete IACD system. Coronary artery disease was found in 11 and the prolonged Q-T syndrome in 1. The average ejection fraction was 34%, and 6 patients had severe congestive heart failure (New York Heart Association class III or IV). The IACD is a completely implantable unit consisting of 2 bipolar lead systems. One system uses a lead in the superior vena cava and on the left ventricular apex through which the cardioverting pulse is delivered. The second system employs a close bipolar lead implanted in the ventricle for sensing rate. After the onset of ventricular tachycardia or fibrillation, the IACD automatically delivers approximately 25 J. Postoperative electrophysiologic study in 10 and spontaneous ventricular tachycardia in 1 patient demonstrated appropriate IACD function and successful conversion in all with an average of 18 +/- 4 seconds. The induced arrhythmias were ventricular tachycardia (160 to 300 beats/min) in 9 and ventricular fibrillation in 1. These data demonstrate that ventricular tachycardia, not ventricular fibrillation, was the predominant rhythm induced during programmed ventricular stimulation in these survivors of cardiac arrest and that the IACD effectively responded to a wide range of ventricular tachycardia rates as well as ventricular fibrillation. Use of the IACD offers an effective means of therapy for some patients who otherwise may not have survived.
Twenty-eight patients who survived multiple arrhythmic cardiac arrest refractory to medical therapy underwent implantation of the automatic defibrillator without additional antiarrhythmic surgery. Lateral thoracotomy was used for implantation in 14 patients and the subxiphoid technique was used in 14. There was no operative mortality and surgical complications were minimal. The longest follow-up was 29 months and the average was 14 months. The implanted device correctly identified and reverted 50 episodes of spontaneous malignant ventricular tachyarrhythmias in six hospitalized patients. After discharge, 20 episodes of automatic out-of-hospital resuscitations occurred in eight patients. Kaplan-Meier survival curves, based on the assumption that out-of-hospital defibrillations would otherwise have been lethal, indicated an expected 1 year mortality of 60 percent. Seven deaths were in fact observed in this period for an actual mortality rate of 30 percent. We conclude that automatic defibrillation is clearly feasible in man and appears to increase survival in selected high-risk patients.
Fifty-two patients who survived several arrhythmic cardiac arrests had implantation of an automatic defibrillator along with additional cardiovascular surgery as indicated. The mean follow-up was 14.4 months and the longest was 3 years. In the hospital, the implanted devices identified and reverted 82 episodes of spontaneous and 81 of 99 episodes of induced malignant tachyarrhythmias. There were 62 automatic resuscitations in 17 patients outside the hospital. Twelve patients died; four of the deaths were not witnessed. These deaths represent a 22.9% total and 8.5% sudden-death 1-year mortality rate. Because the expected 1-year mortality in patients without the automatic defibrillator was calculated to be 48%, there was an estimated 52% decrease in anticipated total deaths. The automatic implantable defibrillator can identify and correct potentially lethal ventricular tachyarrhythmias, leading to a substantial increase in 1-year survival in properly selected high-risk patients.
Since February, 1980, 65 survivors of multiple arrhythmic cardiac arrests unresponsive to therapy were referred for implantation of the automatic defibrillator. In 37 patients (Group I), automatic defibrillator implantation alone was performed by subxiphoid insertion (20 patients) or thoracotomy (17 patients). In another 28 patients (Group II), implantation was combined with definitive cardiac procedures--coronary artery bypass grafting in seven patients, bypass grafting and mitral valve replacement in four patients, and left ventricular aneurysmectomy with endocardial resection in 17 patients. There were no surgical deaths in Group I; four operative deaths occurred in Group II. The longest follow-up has been 34 months, average 15.6 months. Following hospital discharge, 44 episodes of automatic out-of-hospital resuscitation were observed in 11 Group I patients. Similarly, four resuscitations were observed in two Group II patients. Hypothetical survival curves based on the assumption that these out-of-hospital resuscitations were lifesaving indicated expected 1 year survivals rates of 45% in Group I and 85% in Group II. Excluding the perioperative deaths that were unrelated to the defibrillator, the actual 1 year survival rates observed were 75% and 95% in Groups I and II, respectively. Although definitive operation markedly reduced the number of out-of-hospital arrhythmic episodes, the automatic defibrillator appears to increase survival both when implanted alone and when used in combination with cardiac procedures.
The effectiveness and safety of oral flecainide for suppression of complex ventricular arrhythmias was tested in nine patients in a short-term (4 wk), single-blind, placebo-controlled experiment. The prevalence of multiform premature ventricular complexes (PVCs), couplets and nonsustained ventricular tachycardia (VT) (less than 3 PVCs at rate less than 100/min) was determined by 48-hr Holter monitoring on placebo and flecainide (200 to 300 mg b.i.d.) therapy. Multiform PVCs/hr were reduced by 96% in eight of nine patients (P less than 0.001). Couplets per 24-hr period were suppressed entirely in six patients (P less than 0.001). Couplets per 24-hr period were suppressed entirely in six patients (P less than 0.001) and reduced by 92% in the remaining two patients. VT runs per 24 hr were abolished in six patients (P less than 0.02) and reduced by 91% in one. As a group the frequency of PVCs per hour, couplets per 24 hr and VT per 24 hr was reduced by 96% (P less than 0.01) over than in the preceding placebo period. Flecainide (P less than 0.02) slowed heart rate by 10% and prolonged PR, QRS, and QTc intervals by 31%, 47% and 6%. No hematologic, hepatic, or renal abnormalities were found. Side effects were mild, transient, and central nervous system related; blurring of vision was the most frequent effect and was reported in four patients.
To investigate the accuracy of the 12-lead ECG in localizing the site of coronary artery narrowings, we reviewed abnormal ECGs obtained during myocardial infarction, spontaneous angina or exercise stress testing in 134 patients with angiographically documented one-vessel disease. The presence of Q waves, ST-segment elevation and T-wave inversion in leads I, aVL and V1--V4 were all highly correlated with the presence of left anterior descending coronary artery disease (p less than 0.001), and the same ECG findings in leads II, III and aVF were associated with right (RCA) or circumflex coronary artery (LCx) narrowings (p less than 0.001). In contrast, ST depression alone was not useful in predicting the site of coronary artery narrowing. Q waves correctly identified the location of the coronary disease in 98% of cases, ST elevation in 91%, T-wave inversion in 84%, and ST depression in 60%. No electrocardiographic criteria distinguished RCA from LCx disease, even in patients with a right-dominant circulation. These findings should lead to a better understanding of the value and limitations of the 12-lead ECG in localizing coronary artery disease.
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The value of stress thallium-201 scintigraphy for detecting individual coronary arterial stenoses was analyzed in 141 patients with angiographically proved coronary artery disease, 101 with and 40 without a previous myocardial infarction. In patients without infarction, the sensitivity for detecting greater than 50 percent narrowing in the left anterior descending, the right and the left circumflex coronary artery was 66, 53 and 24 percent, respectively. In those with a previous infarction, the sensitivity for demonstrating disease in the artery corresponding to the site of infarction was 100 percent for the left anterior descending, 79 percent for the right and 63 percent for the left circumflex coronary artery. In patients with a prior anterior infarction, concomitant right or left circumflex coronary arterial lesions were detected in only 1 of 12 cases, whereas in those with previous inferior or inferolateral infarction, the sensitivity for left anterior descending coronary artery disease was 69 percent. Because of the reasonably high sensitivity for detecting left anterior descending arterial disease, irrespective of the presence and location of previous infarction, myocardial scintigraphy was useful in identifying multivessel disease in patients with a previous inferior infarction. However, because of its relative insensitivity for right or left circumflex coronary artery disease, scintigraphy proved to be a poor predictor of multivessel disease in patients with a prior anterior infarction and in patients without previous myocardial infarction.
To determine the usefulness of thallium-201 scintigraphy for identifying left main coronary artery disease, the results of scintigraphy at rest and during exercise were compared in 24 patients with 50 percent or greater narrowing of the left main coronary artery and 80 patients with 50 percent or greater narrowing of one or more of the major coronary arteries but without left main coronary involvement. By segmental analysis of the scintigrams, perfusion defects were assigned to the left anterior descending, left circumflex or right coronary artery, singly or in combination, and the pattern of simultaneous left anterior descending and circumflex arterial defects was used to identify left main coronary artery disease. Of the 24 patients with left main coronary artery disease, 22 (92 percent) had abnormal exercise scintigrams. Despite this high sensitivity, the pattern of perfusion defects was not specific; the "left main pattern" was found in 3 patients (13 percent) with left main coronary artery disease but also in 3 (33 percent) of 9 patients with combined left anterior descending and left circumflex arterial disease, 4 (19 percent) of 21 patients with three vessel disease and 3 (6 percent) of 50 patients with one or two vessel disease but excluding the group with left anterior descending plus left circumflex arterial disease. The pattern of perfusion defects in the patients with left main coronary artery disease was determined by the location and severity of narrowings in the coronary arteries downstream from the left main arterial lesion. Concomitant lesions in other arteries were found in all patients with left main coronary disease (one vessel in 1 patient, two vessels in 7 patients and three vessels in 16). For this reason, it is unlikely that even with improvements in radiopharmaceutical agents and imaging techniques, myocardial perfusion scintigraphy will be sufficiently specific for definitive identification of left main coronary artery disease.
Sixty-one medically treated patients had coronary and left ventricular angiography and 24-hour electrocardiographic monitoring 10-24 days after myocardial infarction, and then had serial 24-hour electrocardiographic monitoring during the 13 +/- 11 months after myocardial infarction. Complex ventricular arrhythmias (2 or more sequential ventricular premature depolarizations (VPDs), multiform VPDs, bigeminy) during follow-up were associated with a high mortality rate and occurred most commonly in the setting of three-vessel coronary disease, proximal left anterior descending coronary disease and low left ventricular ejection fraction. By contrast, patients without complex VPDs in either the late hospital or posthospital phase of myocardial infarction had no mortality during the year following myocardial infarction; furthermore, these patients had a higher incidence of single-vessel coronary disease and less left ventricular dysfunction. These results emphasize the adverse prognostic significance of complex ventricular arrhythmias in the year after myocardial infarction and their association with extensive coronary artery disease and left ventricular damage.
The automatic implantable defibrillator is an electronic device designed to detect and promptly correct malignant ventricular arrhythmias. Nineteen patients, all survivors of multiple cardiac arrests because of ventricular arrhythmias unresponsive to therapy, have undergone implantation of the automatic defibrillator. In seven patients who had had a previous cardiac operation, implantation was performed through a left lateral thoracotomy. A median sternotomy was used in five patients without a previous operation. In six patients cardiac procedures were performed concomitantly with defibrillator implantation. There were no operative deaths. The average follow-up is 6 months, the longest being 14 months. Following implantation, 47 episodes of malignant ventricular arrhythmias were documented. Twenty-six occurred spontaneously (17 of them outside the hospital); all were corrected with a single 25 joule pulse. Seventeen of 21 arrhythmias induced postoperatively were terminated. Although further validation is required, this study demonstrates that the automatic defibrillator is capable of diagnosing and terminating potentially lethal ventricular arrhythmias. Finally, implantation can be safely accomplished in an exceedingly high risk population.
Survival, subsequent myocardial infarction and current anginal status were determined for 90 nearly consecutive patients who underwent coronary arteriography at the Johns Hopkins Hospital between 1960 and 1967. All patients had at least one coronary arterial narrowing equal to or greater than 70 percent; 78 of 90 patients would be candidates for coronary bypass surgery by present criteria. Twenty-nine of the 78 surgically "suitable" patients died of cardiac causes; 7 of 49 survivors sustained an acute myocardial infarction (mean follow-up period 9.9 years). Patients with a 70 percent or greater narrowing proximal to the first septal branch of the left anterior descending coronary artery had a significantly greater mortality compared with patients with equivalent narrowing distal to the first septal branch or with patients without 70 percent or greater narrowing of the left anterior descending artery. The patients with a 70 percent or greater narrowing of the left anterior descending artery who died were those with a significant narrowing in at least one other major coronary artery. Multivariate stepwise discriminate function analysis of all clinical, electrocardiographic (except stress electrocardiographic) and arteriographic variables identified three independent predictors of mortality: (1) the simultaneous occurrence of a narrowing in left anterior descending and right coronary arteries, (2) prior myocardial infarction; and (3) 70 percent or greater narrowing proximal to the first anterior descending septal branch. When stress electrocardiographic findings were included, a "positive" stress electrocardiographic test was also an independent predictor of mortality.
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Patients who survive an acute myocardiac infarction (AMI) have significant coronary disease and are at risk for angina pectoris, recurrent myocardiac infarction and sudden death. This study provides data gathered prospectively for 106 patients surviving myocardial infarction who had coronary arteriography, left ventriculography and 24-hour electrocadiographic recordings before hospital discharge and were followed 30 months. Univariate analysis showed that low ejection fraction, proximal left anterior descending coronary disease and significant disease in all three coronary arteries were associated with a high risk of sudden cardial death. The ECG location or type of infarction was not helpful in predicting mortality, reinfarction or continuing angina. Multivariate analysis of 30 clinical and laboratory variables identified previous myocardial infarction and an ejection fraction less than 40% as the best predictors of mortality; all 13 patients who died were identified by these two variables. Three-vessel coronary artery disease, proximal left coronary disease and complicated late hospital-phase ventricular arrhythmias did not provide additional information about mortality once the information provided by the first two variables was considered. Multivariate analysis identified hypertension, three-vessel coronary disease, postinfarction angina pectoris and previous AMI as significant predictors of recurrent AMI during the 30 month follow-up.
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