Revascularization strategies in women with ischemic heart disease.
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Publications and source records attributed to L Mickleborough.
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Primary pericardial mesothelioma is a rare tumour, often discovered late in a patient's clinical course or at autopsy. Antemortem diagnosis is usually made at the time of surgery. A patient who presented with what appeared to be viral pericarditis in October 1997 is reported. Recurrent symptoms prompted re-evaluation with echocardiography, chest computed tomography, magnetic resonance imaging, cardiac catheterization and a diagnosis of constrictive pericarditis. Associated hepatic dysfunction was found to be secondary to congestion. After operative pericardiotomy and histological examination, primary pericardial mesothelioma was diagnosed. The lesion was surgically debulked.
Controversy exists as to whether the unipolar or bipolar electrode configuration is superior in detecting local activations during cardiac mapping studies. However, the strengths and weaknesses of each mode suggest that they may provide complementary information. To examine the relative merits of unipolar and bipolar electrode configurations, recordings by each were simultaneously acquired during episodes of ventricular tachycardia in eight consecutive patients undergoing map guided arrhythmia surgery. Unipolar electrograms were classified as either unambiguous or ambiguous according to whether or not they were polyphasic in nature. The activation times from the unambiguous electrograms were compared with activation times from the corresponding bipolar signals where local activation was measured both at the signal's peak amplitude (BI-PK), and at the point at which the waveform's first major, rapid transient crossed baseline (BI-TRN). Occurrences of discrete diastolic activations were also quantified from the unipolar and bipolar tracings. From a total of 415 unipolar electrograms, 301 unambiguous signals were identified as suitable for comparison with the bipolar signals. Both BI-PK and BI-TRN criteria for the determination of local activation were highly correlated with and not significantly different from the local activation from the unipolar electrogram. From 85 ambiguous unipolar electrograms, it was possible to determine local activation from the corresponding bipolar signal in 33% of the occurrences. From the eight patients, 64 diastolic potentials were recorded of which 42 were seen only in bipolar mode, 7 in only unipolar mode, and 15 were evident in both tracings. The prevalence of diastolic potentials was significantly greater in recordings made using bipolar mode. The results demonstrate that complementary information regarding local activations and diastolic potentials can be derived from unipolar and bipolar recordings and suggest that both electrode configurations should be used in multichannel cardiac mapping systems.
OBJECTIVES: This study was conducted to characterize the functional nature of the reentrant tract responsible for ventricular tachycardia due to ischemic heart disease. BACKGROUND: A zone of slow conduction forming the return path is though to form a critical component of the reentrant mechanism in ventricular tachycardia. Despite its importance, detailed knowledge of the return path is rare in clinical studies. METHODS: Multielectrode arrays were used intraoperatively to obtain unipolar and high gain bipolar recordings of left ventricular endocardium in patients undergoing map-directed surgical ablation of ventricular tachycardia. A total of 224 local electrograms were analyzed for each tachycardia. RESULTS: Of 10 consecutive patients undergoing intraoperative cardiac mapping, detailed recording of the return tracts of eight ventricular tachycardias were obtained in three patients. The recordings demonstrated that return tracts can be complex and extensive, with multiple paths of entry and exit. Potential and actual alternate paths were observed. Spontaneous and induced block occurred within portions of the complex. Intermittent block in one of two paths of entry resulted in intermittent cycle length changes of the tachycardia without a change in configuration. Block in one exit path resulted in a shift to alternative exit paths, with dramatic changes in ventricular activation and tachycardia configuration. Termination of the tachycardia could result from block close to the entrant or exit portion of the return tract. Different tachycardias were seen to share common portions of a return tract. CONCLUSIONS: These observations enlarge and extend our knowledge of the functional repertoire of complex reentrant tracts that occur in infarct-related ventricular tachycardia. The use of common portions of a reentrant tract by several tachycardias is confirmed. Utilization of alternate pathways can account for changes in configuration and cycle length. Spontaneous and induced block can occur at points of entry and exit in a reentrant tract and may identify optimal targets for ablation attempts. Further advances will require greater emphasis on diastolic activation mapping.
Ventricular tachycardia following myocardial infarction in man is thought to be due to a reentrant mechanism, with a zone of slow conduction forming the critical element of the return pathway. Cardiac mapping has helped characterize the anatomical and functional nature of reentrant pathways, and is used to direct antiarrhythmic surgery and catheter ablation. This review will explore how cardiac mapping has contributed to our understanding of reentrant ventricular tachycardia. The role of diastolic mapping will be emphasised, and the implications for future management of ventricular tachycardia discussed.
OBJECTIVES: Four patients with previous repair of tetralogy of Fallot and ventricular tachycardia underwent map-guided surgery to ablate the arrhythmias. BACKGROUND: Although patients with repaired tetralogy of Fallot are at increased risk of sudden death due to ventricular tachycardia, little is known of the origin and mechanism of this arrhythmia. METHODS: A customized right ventricular balloon with 112 electrodes was used to record endocardial activation and, where possible, simultaneous epicardial recordings were obtained with a sock electrode array. Three patients had an aneurysm of the right ventricular outflow tract and one had a septal aneurysm. All had moderate to severe pulmonary valve insufficiency. Preoperative electrophysiologic study demonstrated inducible rapid (cycle length 180 to 300 ms) hemodynamically unstable monoform ventricular tachycardias. RESULTS: Intraoperatively, five different tachycardias (two in one patient) were induced and mapped. The sites of earliest activation were located in the subendocardium of the right ventricular outflow tract in all, but they varied widely among the septum, free wall and parietal band and could not be identified by visible scar. All were due to a macroreentrant circuit initiated by a critical delay in activation beyond a functional arc of block. Two patients treated by cryoablation while the heart was beating and perfused at normal temperature had inducible ventricular tachycardia postoperatively. In the two subsequent patients, the application of cryoablation under anoxic cardiac arrest resulted in noninducibility of arrhythmia. CONCLUSIONS: Ventricular tachycardia in tetralogy of Fallot in these four patients was caused by macroreentry in the right ventricular outflow tract. Surgical success depends on detailed mapping and cryoablation under anoxic cardiac arrest. In patients at risk of sudden death, map-directed surgery may offer distinct advantages over either implantable devices or drug therapy.
OBJECTIVE: The purpose of this study was to obtain improved detection and characterization of reentrant circuits in the infarcted human ventricle. BACKGROUND: The return path of reentrant ventricular arrhythmias usually is not manifested in clinical mapping studies but is thought to be formed by isolated bundles of surviving myocytes whose presence is difficult to detect by standard recording techniques. METHODS: We obtained simultaneous unipolar and high gain bipolar recordings using a left ventricular endocardial balloon array in 10 patients with chronic ischemic heart disease undergoing intraoperative mapping of ventricular tachycardia. RESULTS: Three patients demonstrated seven separate ventricular tachycardias that utilized a return tract that was manifested on up to 20% of all left ventricular electrode sites. The recordings suggested an extensive sheet of surviving myocardial fibers with multiple entry and exit points allowing for different reentrant paths at different times all in the same heart. In one patient, five different ventricular tachycardias could be induced, four of which utilized such a sheet. Two of these tachycardias had the same exit point (site of origin) but two different entry points with a long and short return path resulting in long and short tachycardia cycle lengths. The same sheet sustained another tachycardia with one entry and two exit points resulting in two separate "sites of origin" on the endocardium. Such sheets also were seen to insert into the left bundle system. In one patient portions of the sheet could be detected epicardially. CONCLUSION: The existence of such a structure of surviving myocardium with functional pleomorphism may account for unexplained changes in tachycardia cycle length, epicardial entrainment and spontaneous morphologic changes during ventricular tachycardia.
We evaluated the accuracy of the non-imaging nuclear probe for measuring various parameters of left ventricular function by comparing these with simultaneous measurements acquired via tantalum marker cine-fluoroscopy. Eight patients with surgically implanted mid-myocardial tantalum markers were studied during cardiac catheterization. High temporal resolution tantalum marker-derived volume/time curves were generated and calibrated to absolute endocardial volumes by comparison with contrast left ventricular angiography. Left ventricular function parameters were acquired at baseline and during atrial pacing, nitroprusside infusion and volume loading. Simultaneous measurements obtained with the nuclear probe and via tantalum marker cine-fluoroscopy were compared. The following correlation coefficients were obtained: ejection fraction, r = 0.49, P less than 0.001; peak ejection rate, r = 0.41, P less than 0.01; mean ejection rate, r = 0.62, P less than 0.001; time to peak ejection, r = 0.73, P less than 0.001; peak filling rate, r = 0.73, P less than 0.001; time to peak filling, r = 0.58, P less than 0.001. Relative changes in end-diastolic volume were accurately tracked by the nuclear probe in six of seven patients (r values 0.77-0.93). These results suggest that measurements of certain left ventricular volume parameters with the nuclear probe may not accurately reflect true volume changes as measured by tantalum marker cine-fluoroscopy. Although, the probe may be useful in tracking relative changes in end-diastolic volume, we would advise caution in using this instrument for studies requiring accurate measurements of ejection and filling parameters.
Twenty-six healthy mixed-breed dogs (25 to 35 kg) underwent hypothermic (27 C) cardiopulmonary bypass. The heart was arrested with cold (4 C) cardioplegic solution, and left ventriculostomy performed. Postoperative mortality was 11.5% (3/26). Two deaths were attributable to ventricular fibrillation the night after surgery, and one death 2 weeks later was the result of pulmonary embolization. All other dogs recovered promptly and were well at follow-up evaluation 6 weeks later. The most important considerations were (1) the surgical approach, ie, combining left lateral thoracotomy with cannulation of the right atrium and left femoral artery for cardiopulmonary bypass (CPB) (avoiding median sternotomy and aortic arch perfusion), (2) the adherence to strict criteria for CPB perfusion, consisting of blood flow of at least 2.2 L/m2/min, PCV no less than 25%, gas flow through the oxygenator (97% O2, 3% CO2) of at least 3.5 L/min, maintenance of a mean arterial blood pressure greater than 60 mm of Hg, and heparinization to maintain activated clotting time over 480 seconds, (3) the use of dipyridamole infusion to preserve platelets during CPB, resulting in decreased postoperative blood loss and (4) the monitoring of cardiac, respiratory, renal, and neurologic functions before, during, and after the operation, with particular emphasis on fluid balance and electrolytes. We concluded that a high success rate is possible for open-heart surgery in the dog requiring cardiopulmonary bypass, but only through meticulous surgical technique and the combined application of many monitoring techniques, with timely intervention to correct serious departures from homeostasis.
Thirty-five patients with ischemic heart disease and ventricular arrhythmias underwent intraoperative activation mapping at the time of coronary artery bypass surgery. During ventricular tachycardia, the sequence of activation in the intact ventricle was recorded simultaneously from 110 endocardial or 110 epicardial sites, or both. A balloon array of electrodes, inserted across the mitral valve, was used to obtain endocardial recordings in the left ventricle, and this appeared to facilitate the induction of ventricular tachycardia. Of 61 episodes of tachycardia, 16 (15 patients) were recorded with the epicardial sock and 45 (20 patients) with the additional use of the endocardial balloon. The sequence of activation during tachycardia was observed to conform to one of four configurations: monoregional spread was the most common activation sequence recorded on both the endocardium and epicardium, while biregional activation and figure eight sequences were recorded exclusively on the epicardium and endocardium, respectively. The fourth sequence was a circular spread of activation observed on both surfaces. Continuous activation throughout the tachycardia cycle length was an infrequent finding. Simultaneous recordings of endocardial and epicardial activation were obtained in 45% of episodes. The sequence of activation recorded on one surface was matched by a similar sequence on the remaining surface in less than half of these. The onset of endocardial activation preceded that of the epicardium in greater than 90% of tachycardia episodes, and the duration of left ventricular endocardial excitation often exceeded that recorded epicardially over both ventricles. The epicardium, however, did appear to be an important determinant of surface electrocardiographic configuration.
Both intraoperative endocardial mapping and surgical ablation for ventricular arrhythmias have until now required a ventriculotomy. Such an incision may be associated with an increase in morbidity and mortality, especially when performed through friable myocardium. A "closed heart" technique of intraoperative endocardial mapping and ablation of ventricular arrhythmias was developed in which a balloon array of 112 electrodes was introduced into the left ventricular cavity by a transmitral approach. The array permitted safe delivery of repeated electrical discharges of up to 150 J at each electrode. In four patients with coronary artery disease and no ventricular aneurysm, this "closed heart" technique was used to map and treat seven distinct ventricular tachycardias. The time taken to map each tachycardia varied from 3 to 13 minutes. Between 100 and 150 J was then delivered at each of 10 to 42 electrode sites, and the ablation procedure took 7 to 16 minutes per patient to complete. One patient died 24 hours postoperatively from preexisting thrombocytopenic purpura. There was no significant deterioration in left ventricular function in the three survivors and all have remained arrhythmia free, without antiarrhythmic agents, for 4 to 11 months. This technique offers a new method of surgical treatment of ventricular tachycardia without ventriculotomy, and is particularly suited to patients without a discernible left ventricular aneurysm.
Between December 1981 and August 1983, percutaneous transluminal angioplasty of saphenous vein grafts was performed in 14 men and 4 women, selected because of recurrent anginal symptoms and graft stenosis. The interval from bypass to angioplasty was 41 +/- 36 months. Of 24 lesions, 9 were at the proximal anastomosis, 13 in the distal segment and 2 in the middle segment of the vein graft. The primary success rate was 79%. Failure to cross the stenosis occurred in three patients and failure to dilate in one. The stenosis was reduced from a mean of 82% +/- 13% to 26% +/- 15%. No patient required emergency coronary artery bypass grafting but two underwent elective grafting after the angioplasty had failed. No patient sustained a Q-wave myocardial infarction and all who had a successful angioplasty were asymptomatic or much improved after the procedure. Angiographic follow-up was available in 12 of 14 patients (86%). Six patients had significant symptoms (Canadian Cardiovascular Society class II to III) and five of these had evidence of restenosis. Among the six patients who were asymptomatic, two had angiographic evidence of restenosis. The overall rate of restenosis was 58% (7 of 12). Repeat angioplasty was successful in three of the five patients in whom it was attempted. The authors conclude that percutaneous transluminal angioplasty of a saphenous vein graft for a localized area of stenosis is effective and safe, but there is a high rate of restenosis that possibly is due to intimal fibrous proliferation in saphenous vein grafts.
Estimation of infarct size utilising the epicardial electrocardiogram has been the subject of considerable controversy. The present study re-examines this technique in a dog model. It demonstrates that epicardial Q waves and S-T elevation are qualitative markers of local necrosis with different degrees of reliability; neither, however, is quantitatively related in a simple linear fashion to extent of necrosis. Conclusions from previous studies have been influenced both by different mathematical analyses of data and the inclusions of nonhomogenous sites in linear regression models.
This study examines the significance of epicardial Q waves as a marker of myocardial cell necrosis. Ischaemia was produced in dogs by two methods: coronary artery occlusion sustained for 24 h (Group 1) and occlusion for 1 h followed by reperfusion (Group 2). Q waves did not appear until after 3 h of sustained occlusion, but were present within 40 min of reperfusion. In both groups, Q waves were not transient but persisted for at least 24 h. CPK levels were determined at 24 h in specimens from each lead site. In Group 1, Q sites had 66.6 +/- 5.9% (mean +/- SEM) less CPK than R wave sites (P less than 0.005). In Group 2, Q sites had only 28.2 +/- 4.5% less CPK than R sites. These results suggest that the extent of necrosis was greater at Q sites with sustained occlusion than with reperfusion. A similar relationship existed for the levels of ATP and CP determined at Q and R sites at 24 h. Histological examination by light and electron microscopy confirmed that in both groups, Q sites corresponded to areas of necrosis, while R sites indicated normal myocardium. However, the type of necrosis depended on the pathogenesis. Our results demonstrated that epicardial Q waves were a reliable marker of cell death, but that the morphological picture and extent of cell death depended on the mechanism and manner of injury. These conclusions were tested in a final series (Group 3) in which propranolol was given before and with release of the occlusion (0.5 mg.kg-1 at each time). In 47 sites at risk, in five dogs only two Q waves appeared. In each of these two, cell death was confirmed by evidence of CPK depletion and morphological alteration. In the remaining sites, no CPK depletion occurred. Histological examination revealed only infrequent small islands of subendocardial necrosis. The results confirm the validity of the epicardial electrocardiographic findings and illustrate the role of propranolol in preventing reperfusion necrosis.
Many of the recommendations presented in this consensus report are summarized in Figure 2. All patients with known or suspected heart failure should undergo a detailed history and physical examination. Other causes for the symptoms and/or clinical signs indicative of heart failure should be excluded. Routine biochemical tests, as well as a standard chest x-ray and ECG, should be performed on all patients with heart failure. Precipitating or aggravating causes of heart failure should be eliminated. Patients with potentially surgically correctable lesions, such as constrictive pericarditis, valvular disease or left ventricular aneurysm, should be referred for cardiological evaluation and the appropriate surgery. Patients with ischemic induced heart failure should be assessed for possible revascularization by either angioplasty or bypass surgery. Pending clinical findings and the degree of systolic or diastolic dysfunction present, determined by noninvasive tests, the panel made recommendations concerning the choice of various therapeutic agents. These clinical guidelines have been developed for practising physicians who manage patients with heart failure. The process by which consensus recommendations were developed by the Canadian Cardiovascular Society was based on the principle that guidelines have the best chance of succeeding if they are developed by those who will be using them. Strategies that ensure physicians are aware of the current guidelines, and that their implementation leads to measurable improvement in the diagnosis and management of patients with heart failure must be developed. Consensus reports represent an ongoing process which is subject to revision when further conclusive evidence is obtained by ongoing and future clinical trials.