Michael B. Simson

Right ventricular tachycardia: clinical and electrophysiologic characteristics.

This report describes the clinical and electrophysiologic characteristics of 30 patients without myocardial disease who had ventricular tachycardia with the morphologic characteristics of left bundle branch block and inferior axis. The tachycardias were nonsustained in 24 patients, sustained (greater than 30 sec) in six patients, and provocable by exercise in 14 of 23 patients undergoing a standard Bruce protocol. Ventricular tachycardia was induced during electrophysiologic study in 22 of 30 patients. Programmed stimulation induced tachycardia in 10 of 30 patients, most frequently by rapid atrial or ventricular pacing. Isoproterenol infusion facilitated tachycardia induction in 13 of 23 patients. Endocardial activation mapping, performed in 10 patients, confirmed that earliest ventricular activation during tachycardia occurred at the right ventricular outflow tract on the interventricular septum. These tachycardias were unique in their responsiveness to a wide variety of antiarrhythmic drugs, including type I drugs and propranolol. During a mean follow-up of 30 months, no patient has died or experienced cardiac arrest. Two patients appear to be in spontaneous remission, and no patient has developed additional signs of cardiac disease.

Relation Between Late Potentials on the Body Surface and Directly Recorded Fragmented Electrograms in patients With Ventricular Tachycardia

The relation between low-amplitude, late potentials on the body surface and directly recorded electrograms in 8 patients with and 11 patients without ventricular tachycardia (VT) was studied. Bipolar X,Y,Z leads were signal-averaged and filtered with a digital technique. All patients had catheter endocardial left ventricular maps. The VT group had medically intractable VT and an endocardial excision was performed for control of VT. Before bypass, epicardial maps were obtained in the operating room. All studies were performed during normal sinus rhythm. Four patients without VT, each with a previous myocardial infarction, had fragmented endocardial electrograms recorded at 2.0 +/- 1.2 sites. The latest electrogram for each patient ended 87 +/- 8 ms after QRS onset, within the high-amplitude portion of the filtered QRS complex. All patients with VT had fragmented electrograms recorded at 6.1 +/- 3.1 sites/patient. Eighty-eight percent of the fragmented electrograms were endocardial. The latest fragmented electrogram for each patient ended 161 +/- 43 ms after QRS onset, significantly later than the fragmented electrograms from the patients without VT (p = 0.002). Six VT patients had low-amplitude, late potentials at the end of the filtered QRS complex. In these patients, the last 40 ms of the filtered QRS complex contained a higher proportion of fragmented electrograms compared with earlier segments of the QRS complex (68% versus 27%, p less than 0.001). Two patients with VT did not have late potentials. One patient with left bundle branch block had delayed left ventricular epicardial activation which masked the fragmented electrograms. The other had fragmented electrograms of brief duration which ended 80 +/- 12 ms after QRS onset, during the time of normal ventricular activation. It is concluded that the late potential corresponds to delayed, fragmented electrographic activity. Failure to record a late potential may arise from delayed ventricular activation at other sites from bundle branch block or fragmented electrograms of a brief duration.

Results of signal-averaged electrocardiography and electrophysiologic study in patients with nonsustained ventricular tachycardia after healing of acute myocardial infarction.

Programmed stimulation and signal-averaged electrocardiography were performed in 43 consecutive patients with nonsustained ventricular tachycardia (VT) after healing of inferior (29 patients) or anterior wall (14 patients) acute myocardial infarction. Twenty-two patients had inducible sustained VT. Patients with inferior infarction and inducible sustained VT had significantly longer filtered QRS durations (125 +/- 19 vs 112 +/- 15 ms, p less than 0.01) and significantly lower voltage in the last 40 ms of the filtered QRS complex (19 +/- 5 vs 30 +/- 14 microV, p less than 0.05) than those without inducible sustained VT. In contrast, the signal-averaged electrocardiographic measurements in patients with anterior infarction and inducible sustained VT did not differ significantly from those without inducible sustained VT. The results of these studies were compared with those of 2 control groups: 45 patients without ventricular arrhythmias after myocardial infarction and 95 patients with spontaneous and inducible sustained VT after myocardial infarction. The signal-averaged electrocardiographic measurements in patients with spontaneous nonsustained VT after inferior infarction were intermediate between the control group without arrhythmias and the control group with sustained VT. The signal-averaged electrocardiograms in patients with nonsustained VT after anterior infarction were not significantly different from those in patients without ventricular arrhythmias. The study shows that the site of infarction influences the signal-averaged electrocardiogram in patients with VT after myocardial infarction. The signal-averaged electrocardiogram may be useful in identifying patients with nonsustained VT after a remote inferior myocardial infarction who have inducible sustained VT.

Relation of late potentials to site of origin of ventricular tachycardia associated with coronary heart disease

Signal-averaged electrocardiograms and endocardial catheter mapping were performed in 41 patients with coronary artery disease and sustained ventricular tachycardia (VT) to determine the relation between signal-averaged late potentials (SA-LPs) and catheter-mapped late activity (CM-LA) to the site of origin of VT. The 41 patients had 79 morphologically distinct VTs. Either CM-LA or SA-LP was present during sinus rhythm in 37 of 41 patients (90%). Twenty-two out of 30 patients (73%) had CM-LA corresponding to SA-LP during normal sinus rhythm. Patients with SA-LP had a significantly greater number of sites of CM-LA, which were later and longer in duration than patients without SA-LP present during sinus rhythm. In a select group of patients, those with both SA-LP and CM-LA, the site of origin of VT was located at or adjacent to a site of CM-LA during sinus rhythm in 38 of 44 (86%); however, 36 of 78 sites (46%) of CM-LA were clearly distant from the site of origin of VT. In conclusion, CM-LA corresponding to SA-LP in patients with VT is sensitive but not specific for the site of origin of VT.

Visualization of the distance between perfusion and anoxia along an ischemic border.

The distance between perfusion and anoxia was measured on the border of an experimental ischemic area in the rabbit heart. Reduced nicotinamide adenine dinucleotide (NADH) fluorescence photography was used to detect myocardial anoxia. Fluorescein angiography marked areas of myocardial perfusion. The hearts were isolated, perfused with a hemoglobin-free solution and performed no external work. In all hearts there was a narrow band between areas of perfusion and anoxia that measured 329 ± 42 μ (mean ± SD). The transition from minimal to full NADH fluorescence was abrupt, less than 80 μ. We conclude that the normoxic/anoxic transition is sharp, and the gap between perfusion and anoxia is narrow along an ischemic border in the isolated heart performing no external work. These data suggest that in the in vivo working heart the gap between perfusion and anoxia would be even narrower.

The mechanism of apparent right bundle branch block after transatrial repair of tetralogy of Fallot.

The electrocardiographic pattern of right bundle branch block (RBBB) is routinely observed after transatrial repair of tetralogy of Fallot even though no ventriculotomy has been performed. The mechanism of this conduction disturbance was studied in 16 patients with tetralogy of Fallot and one patient with infundibular pulmonic stenosis. Preoperative ECGs and vectorcardiograms showed right ventricular hypertrophy and no RBBB. Epicardial activation maps were obtained before and after total surgical repair in all patients and after infundibular resection but before closure of ventricular septal defect (VSD) in four of these patients. After infundibular resection, RBBB appeared and activation was markedly delayed (> 30 msec) over the pulmonary outflow tract, but was unchanged over the body of the right ventricle. No further changes in ventricular activation occurred after closure of the VSD. This study shows that RBBB after transatrial repair of tetralogy of Fallot is usually produced by infundibular resection, but not by VSD closure, and is associated with delayed activation of the pulmonary outflow tract and base of the right ventricle which results from damage to portions of the right ventricular conduction system.

Temporal relation between onset of cell anoxia and ischemic contractile failure: Myocardial ischemia and left ventricular failure in the isolated, perfused rabbit heart

Contractile dysfunction is characteristic of the acutely ischemic myocardium. This study was undertaken to assess the temporal relations between the onset of cell anoxia and ischemic contractile failure in isolated, isovolumetric contracting rabbit hearts. High speed epicardial fluorescence photography using reduced nicotinamide adenosine nucleotide (NADH) was used to identify areas of cell anoxia. The onset of ischemia was correlated with deterioration of pressure generation over the course of sequential 60 second coronary arterial occlusions. In the isovolumetric contracting rabbit heart, areas of ischemia were detected 2 seconds after coronary occlusion. Significant reduction in peak systolic pressure occurred at 6 seconds of ischemic time and pressure continued to decrease throughout the 60 second period of coronary occlusion. NADH accumulation indicates imbalance of myocardial oxygen supply and demand and the cessation of oxygen utilization by the mitochondria. The results of this study indicate that ischemia is detectable within 1 to 2 seconds after coronary occlusion and that ischemic ventricular dysfunction occurs several seconds thereafter. Myocardial oxygen reserve is negligible.

Alterations in the initial portion of the signal-averaged QRS complex in acute myocardial infarction with ventricular tachycardia

This study was designed to examine 2 hypotheses: that acute myocardial infarction (AMI) alters early cardiac activation measured by signal-averaging; and that the magnitude of abnormality of early activation may be greater in patients with post-AMI ventricular tachycardia (VT). We examined the root-mean square voltage amplitude in 10-ms intervals over the first 80-ms of the signal-averaged QRS complex. Data from 42 healthy volunteers were compared with those from 52 patients with previous AMI (24 anterior) but no VT and 46 post-AMI patients (33 anterior AMI) with recurrent sustained VT. Patients with VT differed from other post-AMI patients because of lower left ventricular ejection fraction, more frequent aneurysm formation and higher levels of ventricular ectopic activity. A significant decrease in initial voltage amplitude occurred at 30 to 40 ms after the beginning of the QRS in both anterior and inferior AMI patients compared with the normal group. A further significant decrease in initial amplitude occurred in VT patients both after anterior and inferior AMI. These differences persisted for the remainder of the 80-ms interval. These changes were weakly related to QRS duration (r = 0.45), ejection fraction (r = 0.50) and poorly correlated with the presence of Q waves on 12-lead electrocardiogram (r = 0.21). Direct endocardial catheter recordings performed in VT patients confirmed abnormalities of local septal activation after anterior and inferior AMI.(ABSTRACT TRUNCATED AT 250 WORDS)

Pharmacologic modification of myocardial ischemia.

The value of three agents in reducing the area of myocardial ischemia in rabbit hearts perfused with crystalloid solution was examined. Ten hearts received crystalloid solution with methylprednisolone (M), 0.25 mg/ml; 18 with hyaluronidase (H), 4 U/mi; and 10 with propranolol (P), 1 g.g/ml. Thirty-six hearts served as controls. The mitral valves were excised, the hearts were paced at 240 beats/min and a coronary artery was ligated. The ischemic area was evaluated by nicotinamide adenine dinucleotide autofluorescence photography, an intrinsic, high-resolution display of anoxic tissue. The ischemic area was determined by computer from standardized photographs. Myocardial oxygen consumption (MVO2) was determined and photographs were taken before and at 10-minute intervals after ligation. At 60 minutes, each heart was perfused with rhodamine dye and quick-frozen. In hearts treated with M and H, coronary blood flow increased by 151% (51.7 ± 3 to 77.9 ± 3 ml/min) and 150% (48.3 ± 2 to 72.3 ± 2 m/min), respectively (p < 0.001), whereas in hearts treated with U and P, coronary flow decreased at 60 minutes. In the control hearts, the ischemic area did not change between 5 and 40 minutes of ischemia. The ischemic area of H-treated hearts decreased from 136 ± 4 mm2 to 110 ± 9mm2 between the postligation control and the end of the experiment (p < 0.01). The ischemic area of M-treated hearts decreased from 131 ± 5 mm2 to 113 ± 5 mm2 (p < 0.05). P produced no change in ischemic area (p > 0.4). There was no change in the oxygen-diffusion zone of P-treated or control hearts (439 ± 13 vs 383 ± 12, c, p > 0.1). The oxygendiffusion zone between perfused and anoxic tissue in the M and H hearts increased from 383 ± 12, u to 861 ± 76, u and 681 ± 62, i, respectively (p < 0.001). We conclude that significant volumes of myocardium remain normoxic within nonperfused areas of M-, P- and H-treated hearts.

Changes in cardiac excitability and vulnerability in NMR fields

Alterations in ventricular excitability and vulnerability were assessed in nine isolated perfused rabbit hearts in and out of static external magnetic fields (4.7 tesla) associated with radiofrequency pulsing (5 gauss). Ventricular refractoriness was assessed with the strength interval relationship in and out of the NMR magnet. Strength interval curves were measured at threshold, at the midpoint of the strength interval relationship, and at 10 mA. The refractory period measured at threshold was 193 +/- 24 mS outside the magnet and 195 +/- 24 mS inside the magnet (P = ns). Ventricular refractoriness measured at the midpoint of the strength interval curve was 169 +/- 16 mS outside and 167 +/- 17 mS in the magnet (P = ns). At 10 mA the refractory period outside of the magnet was 162 +/- 16 mS and 161 +/- 17 mS in the magnet (P = ns). To assess ventricular vulnerability the repetitive response threshold and the ventricular fibrillation threshold were also determined in and out of the NMR magnet. The repetitive response threshold was 61 +/- 16 mA out of the magnet and 75 +/- 24 mA inside the magnet. This was significant at the P = 0.04 level. The ventricular fibrillation threshold was 71 +/- 14 mA out of the magnet and 81 +/- 20 mA in the magnet (P = ns). In summary, static magnetic fields associated with radiofrequency pulsing have no measureable effect on the strength interval relationship. There is no increase in ventricular vulnerability as assessed by the repetitive response threshold and the ventricular fibrillation threshold.