Programmed electrical stimulation of the heart in coronary artery disease.
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Biomedical subjects
Publications and source records attributed to T Meinertz.
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The influence of the autonomic nervous system on sinus node automatism was assessed in 61 patients with suspect sinus node dysfunction. Cardiac frequency and corrected sinus node recovery time (CSNRT) were determined before and after functional autonomic blockade with intravenously administered propranolol (0,2 mg/kg) and atropine (0,04 mg/kg). A pathologic CSNRT was found in 59% of patients before and in 54% after autonomic blockade. In 44% pathologic CSNRT occurred during both conditions. In these patients intrinsic sinus node disease can be assumed. In 15% of patients an initially pathologic CSNRT became normal after blockade. In these patients sinus node dysfunction is caused by autonomic dysregulation. In 10% of patients pathologic CSNRT was seen for the first time after blockade. In such patients an altered autonomic balance seems to camouflage the primary intrinsic sinus node disease. Abnormal intrinsic cardiac frequency (cardiac frequency after autonomic blockade) was observed in pathologic prolongation of CSNRT after blockade, however not in normal CSNRT. On the other hand only 39% of patients with prolonged CSNRT after blockade had at the same time an abnormal intrinsic cardiac frequency. Autonomic blockade improves the diagnosis of the sick sinus node syndrome. Demonstration of abnormal intrinsic cardiac frequency is highly specific of intrinsic sinus node disease. Normal intrinsic cardiac frequency does, however, not exclude intrinsic sinus node disease.
We determined the incidence of repetitive ventricular response (RVR) after programmed electrical stimulation and the incidence of spontaneous ventricular arrhythmias during 24 hr Holter monitoring in 38 patients in whom extensive non-invasive and invasive diagnostic tests had excluded abnormalities suggestive of organic heart disease. A standardized stimulation protocol with single (S1S2) and double (S1S2S3) extrastimuli during ventricular drive at cycle lengths of 600, 500 and 430 msec with a current strength below 5 mA at the right ventricular apex was employed. RVR occurred in 20 patients (58%) after S1S2 and in 30 patients (79%) after S1S2S3 stimulation. Eighteen patients (47%) showed RVR with 2 echo beats and 1 patient had 3 echo beats. RVR was due to bundle branch reentry (BBR) in 20 patients independent of the mode of stimulation. RVR due to intraventricular reentry (IVR) was found in 17 patients (47%) only after S1S2S3 stimulation. The incidence of both BBR and IVR was influenced by the basic ventricular driving rate, decreasing with shorter basic cycle lengths. 17 patients had no ventricular premature depolarizations (VPDs), 12 patients had uniform, 4 multiform (Lown III), 2 consecutive (Lown IVA) VPDs, and 1 patient had parasystolic rhythm. There was no relation to the incidence of repetitive ventricular response. We conclude that in patients without identifiable organic heart disease RVR with more than 2 consecutive beats is rarely found if single and double extrastimuli are employed during ventricular drive. Both bundle branch and intraventricular reentry with one or two echo beats are a common finding in this population without relation to the incidence of spontaneous ventricular arrhythmias.
The fibrinolytic efficacy and systemic effects on coagulation variables of intracoronary administration of an acylated streptokinase-plasminogen complex (BRL 26921) were assessed in 23 patients with an acute transmural myocardial infarction. The infarct vessel was totally occluded in 22 patients and subtotally stenosed in 1 patient. Reperfusion was achieved in a total of 17 patients (74%), in 2 patients with the use of a guide wire. Reperfusion time in those patients treated with BRL 26921 alone amounted to 42 +/- 37 minutes. Reocclusion occurred in two patients subsequently. Four patients died; in two of these, intracoronary thrombolysis was unsuccessful. Reptilase time increased from 13 +/- 3 to 49 +/- 31 seconds (p less than 0.001), fibrinogen levels decreased from 280 +/- 65 to 126 +/- 76 mg% (p less than 0.001). Factor V decreased from 96 +/- 11 to 53 +/- 26% (p less than 0.001), and factor VIII from 99 +/- 1 to 55 +/- 36% (p less than 0.001). Peripheral hyperplasminemia, defined as a reduction of fibrinogen (less than 100 mg%) with a reduction of factor V and VIII (less than 75%) simultaneously occurred in eight patients. Six (75%) of these 8 patients demonstrated reperfusion, whereas 9 (64%) of 14 patients without peripheral hyperplasminemia were also successfully reperfused. Bleeding complications occurred in two patients who demonstrated hyperplasminemia. Thus, effective intracoronary thrombolysis could be achieved with only minor effects on peripheral coagulation variables in the majority of patients.
Transluminal coronary angioplasty is successfully used in stable and unstable angina. Out of 107 patients admitted with unstable angina 28% were treated medically, 24% operatively and 48% by angioplasty. In a total of 116 patients the stenosis diameter was enlarged from 75.0 +/- 11.0% obstruction to 25.1 +/- 16.4% (improvement 49.9 +/- 16.5%) without differences between concentric and eccentric or right and left coronary stenosis. In 11 out of 22 patients with total coronary occlusion of recent origin the vessel was reopened by the balloon and enlarged to a resting stenosis of 22.3 +/- 16.4%. There were no differences in the success- and the complication rate between stable and unstable angina. After successful thrombolysis residual stenoses greater than 50% are dilated during the same session. In a randomized prospective study 51 patients were dilated immediately (group I) and 48 patients (group II) treated conservatively. In group I the reinfarction- and the cardiac death-rate was two patients compared to seven patients in group II. After four weeks there was one reocclusion (3%) compared to five (17%) and a residual stenosis of 31.9 +/- 24.4% versus 78.0 +/- 15.2%. Angioplasty can be used with good results and a low complication rate in unstable angina and following successful thrombolysis.
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The induction of a repetitive ventricular response (RVR) by programmed electrical stimulation (PES) in patients with malignant ventricular arrhythmias such as ventricular tachycardia or ventricular fibrillation is associated with poor prognosis. However, the incidence and clinical significance of RVR in patients with normal hearts and in those with coronary artery disease (CAD) who do not have a history of malignant ventricular arrhythmias are unknown. In this paper, we present our views on the clinical value of PES in those patients. The incidence of RVR in patients without evidence of heart disease remains controversial. The possible reasons for the disparities between studies are due to differences in the study populations and stimulation protocols used. In 38 patients with normal hearts proven by left ventricular and coronary angiography no patient had three or more ventricular depolarizations in response to PES with single and double premature stimuli. The same stimulation protocol was used in 136 patients with coronary artery disease. The incidence of RVR greater than or equal to 3 (three or more ventricular depolarizations in response to PES) was related to the time interval to prior acute myocardial infarction and to the degree but not to the extent of left ventricular wall motion abnormalities. The relationship between spontaneous ventricular arrhythmias and those induced by PES was compared in 267 patients. Although there was some correlation between absence or presence of both types of arrhythmias, the presence of RVR greater than or equal to 3 did not predict precisely the presence of high grade ventricular arrhythmias during Holter-monitoring. The prognostic significance of RVR greater than or equal to 3 in patients with chronic stable coronary artery disease remains to be determined. However in patients with recent acute myocardial infarction it has been found that subjects at risk of sudden death (SD) can be identified by PES. We feel that until the prognostic significance of RVR is better defined its use as a basis for guiding antiarrhythmic therapy is not warranted.
The technique of closed-chest ablation of the atrioventricular (AV) conduction system was used in 3 patients (53-62 years of age) with atrial flutter not responding to medical management. A persistent third-degree AV block was induced in all patients. Moderate increases in CK and CKMB enzymes but not in Tc-pyrophosphate uptake were observed in these patients. 5 days after the procedure a permanent pacemaker was implanted in each case. We conclude that closed-chest ablation of the AV conduction system is a safe and efficient procedure in selected patients with drug-resistant supraventricular arrhythmias.
The right pulmonary artery (PA) was quantitatively assessed by suprasternal M-mode echocardiography in 25 patients in whom an atrial septal defect (ASD) was suspected clinically. In 10 patients an ASD was excluded (Group 1) and in 15 it was confirmed (Group 2). The smallest diameter of the right PA at end-diastole in Group 1 was 8.8 +/- 1.5 mm/m2 body surface area and in Group 2 14.8 +/- 3.6 mm/m2 (p less than 0.001). The greatest diameter of the right PA during systole was also much smaller in Group 1 (11.3 +/- 1.2 mm/m2) than in Group 2 (17.7 +/- 3.5 mm/m2) (p less than 0.001). The absolute and percent systolic expansion of the right PA did not differ in the 2 groups (2.7 +/- 0.5 mm [29.1 +/- 10.8%] in Group 1 and 2.9 +/- 0.8 mm [20.8 +/- 9.8%] in Group 2). No correlation was found between measured and derived echocardiographic variables of the right PA and the magnitude of the left-to-right shunt. Patients in Group 2, who had an additional pressure elevation in the PA, showed, on average, a larger right PA and a smaller percent systolic expansion. The study demonstrates characteristic alterations in the wall motion pattern of the right PA in patients with ASD, indicating increased pulmonary blood flow.
Eight patients with thoracic aortic aneurysms were investigated by angiography, computed tomography and two-dimensional echography. According to results of computed tomography or angiography six patients had a dissecting aortic aneurysm (five patients type 1 and one patient type 3 according to DeBakey) and two patients had a thoracic aortic aneurysm without dissection. In addition, thrombi in the descending aorta were shown in three patients by computed tomography or by angiography. Type and extent of the aneurysms could be evaluated by two-dimensional echography in all patients. Only in one patient could the origin of dissection in the ascending aorta not be localised precisely by echography. In three patients thrombi in the descending aorta could be demonstrated. For assessment of type and extent of the aneurysm the suprasternal approach was superior to precordial, subcostal and apical imaging. Parasternal investigation resulted in echographic demonstration of dissection in only two cases. Two-dimensional echography is a technically less demanding and useful method in the diagnosis of thoracic aortic aneurysms.
Sixteen patients were investigated by means of programmed atrial stimulation at two different driving rates: 100 and 120/min. All patients had an increased atrial vulnerability at both driving rates. After intravenous flecainide application (1 mg/kg body weight as a bolus followed by the same amount given by infusion over a period of 20 min) the increased vulnerability was abolished in 11 and 9 patients respectively. In the remaining patients the rate of induced atrial tachyarrhythmia decreased. These findings correlate with a significant prolongation of the effective refractory period of the right atrium and a significant shortening of the relative refractory period of the right atrium. It is concluded that flecainide may be effective in the treatment of atrial arrhythmias in man.
The effect of iv digoxin on normal sinus node function was studied after pharmacologic autonomic blockade (AB) in ten patients. Sinus cycle length (SCL), sinus node recovery time (SNRT) and sinoatrial conduction time (SACT) were determined before and after AB with propranolol (0.2 mg/kg body weight) and atropine sulfate (0.04 mg/kg body weight) iv, and 15 min, 30 min, and 45 min after 1 mg iv digoxin. AB resulted in a significant decrease (P less than 0.01) in SCL (916 +/- 158 to 716 +/- 120 ms), in SNRT (1,229 +/- 221 to 871 +/- 190 ms), and in SACT (79 +/- 34 to 44 +/- 10 ms). Fifteen minutes after iv digoxin there was no significant change observed in SCL (716 +/- 120 to 708 +/- 92 ms), in SNRT (871 +/- 190 to 864 +/- 148 ms), or in SACT (44 +/- 10 to 46 +/- 15 ms). Similar results were obtained 30 min after digoxin administration. It is concluded that a single therapeutic dose of digoxin has no direct effect on electrophysiologic parameters of normal intrinsic sinus node function.
Cardiac frequency could not be lowered in a 62-year-old patient with atrial flutter and 2:1 conduction. Using an electrode catheter positioned in the His bundle area an electric current of 80 Ws was effected. A third-degree atrioventricular block developed which regressed after 6 hours. The electrophysiologic assessment after one week showed a marked diminution of AV node conduction capacity.
Of 350 patients who had extensive non-invasive and invasive cardiological diagnostic tests, 56 had completely normal results. 24-hour ECG monitoring of the latter revealed the following ventricular arrhythmias-ventricular extrasystoles (VES): 36% without, 23% with rare ones (less than 30/h), 5.4% with more than 30/h, 25% with polytopic VES, 7.1% with paired VES and 3.6% with ventricular tachycardia. There was no preferential VES pattern. Mean duration of VES was 0.15 s. There were no VES with a prematurity index of less than 1. Extending ECG monitoring to 96 hours (10 persons without heart disease) did not reveal any more significant VES, but registering for less than 24 hours definitely underestimated the frequency of VES in persons without heart disease. In those without angiographic evidence of heart disease 36% had complex and 5.4% frequent VES. Complex arrhythmias, however, are rare in the individual subject and generally not accompanied by frequent VES. Frequent complex arrhythmias or both frequent and complex arrhythmias, as well as VES with a prematurity index less than 1, are suggestive of organic heart disease.
The diagnosis of dilated (congestive) cardiomyopathy was made in 75 patients on the basis of clinical, ECG, echo and angiographic-haemodynamic findings. Ambulatory 24-hour monitoring was undertaken in all patients. Nearly all of them (93%) had ventricular extrasystoles (VES), 35% more often than 1000/24 h. In 15% VES occurred in pairs, in 44% as ventricular tachycardia. In general, frequent VES (greater than 30/h) also came in pairs and/or as ventricular tachycardia. On the other hand, not all patients with such complex arrhythmias also had frequent VES. In about 70% of all patients with ventricular tachycardia such episodes were registered repeatedly, in more than 40% more than five tachycardia episodes per 24 hours. In the majority of patients the tachycardia consisted of three (33%), four (12%) or five (18%) consecutive ventricular complexes. All episodes of ventricular tachycardia ended spontaneously and were clinically largely silent. Apparently there was no clinically relevant correlation between frequency and severity of the arrhythmia, on the one hand, and extent of abnormal ventricular function, on the other. These findings indicate that frequent and complex ventricular arrhythmias are a characteristic feature of dilated (congestive) cardiomyopathy. If they occur in heart disease of seemingly unknown aetiology, dilated cardiomyopathy should be suspected. Preliminary findings of long-term observation indicate that patients with frequent ventricular tachycardias have a higher risk of sudden death.
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A deficiency of selenium is suspected to be involved in the pathogenesis of congestive cardiomyopathy. Therefore the serum selenium content of 20 patients with proven congestive cardiomyopathy was measured and compared to that of a healthy control group. The serum selenium content of the patients with cardiomyopathy was found to be different from that of the healthy control group. The mean value of selenium in serum for the control group was 80.1 micrograms Se/1 (SD +/- 13.2) within a range of 53 and 117 micrograms Se/1. From the 20 patients with congestive cardiomyopathy six patients showed selenium concentrations in the normal value range of the control group; in the serum of 14 patients a distinct lower selenium content was found (mean value 47.8 micrograms Se/1 (SD +/- 16.2)) within a range of 23 and 70 micrograms Se/1. A positive correlation was found between serum selenium content and the left ventricular ejection fraction. Our results suggest that a deficiency of selenium may be present in a number of patients with congestive cardiomyopathy.
The electrophysiologic effects of lorcainide, a class I antiarrhythmic agent with local anesthetic properties, were studied in 20 patients with the Wolff-Parkinson-White syndrome. After intravenous administration of lorcainide (2 mg/kg), the sinus cycle length decreased in all patients from 705 +/- 117 to 636 +/- 94 ms (p less than 0.001). The atrioventricular conduction time lengthened from 84 +/- 22 to 94 +/- 22 ms (p less than 0.01) and the QRS duration increased from 92 +/- 19 to 120 +/- 29 ms (p less than 0.001). The effective refractory period of the atrium increased from 230 +/- 27 to 243 +/- 35 ms (p less than 0.05), whereas the ventricular refractoriness was unaffected. Retrograde conduction over the accessory pathway was blocked in 5 of 18 patients after lorcainide; in the remaining 13 patients a prolongation from 107 +/- 32 to 162 +/- 57 ms (p less than 0.001) was found. Anterograde conduction over the accessory pathway was blocked in 6 patients, and in all other patients it increased considerably. Circus movement tachycardia could be induced in 14 patients before and in 10 patients after the drug. The shortest R-R interval during tachycardia lengthened from 326 +/- 40 to 364 +/- 67 ms (p less than 0.05). The tachycardia zone was unaffected by lorcainide. In 15 patients atrial fibrillation was induced. After lorcainide anterograde conduction during atrial fibrillation was blocked (n = 5). The shortest R-R interval over the accessory pathway during induced atrial fibrillation increased from 228 +/- 35 to 304 +/- 103 ms (p less than 0.05). Intravenous administration of lorcainide produced a pronounced negative dromotropic effect on the conduction properties of the accessory pathway. Lorcainide appears to be a promising new antiarrhythmic agent in patients with the Wolff-Parkinson-White syndrome.