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Biomedical subjects

C L Wolfe

Publications and source records attributed to C L Wolfe.

At least 37 records · Page 2Linked to original sources
PubMed1994

Exposure to environmental tobacco smoke increases myocardial infarct size in rats.

BACKGROUND: Exposure to environmental tobacco smoke (ETS) has been epidemiologically linked to death from ischemic heart disease in nonsmokers. In this study, we evaluated the influence of 3 days, 3 weeks, and 6 weeks of ETS exposure on myocardial infarct size in a rat ischemia/reperfusion model. METHODS AND RESULTS: Sprague-Dawley rats exposed to ETS (four Marlboro cigarettes per 15 minutes, 6 hours per day, 5 days per week) for 3 days (n = 24), 3 weeks (n = 21), or 6 weeks (n = 12) and control rats (n = 24, n = 21, and n = 12, respectively) were subjected to 35 minutes of left coronary artery occlusion and 2 hours of reperfusion. Infarct size and risk area were determined by triphenyltetrazolium chloride and phthalocyanine blue staining, respectively. Air nicotine, carbon monoxide, and total particulates were measured during ETS exposure. Serum lipids, plasma carbon monoxide hemoglobin (COHb), nicotine, and cotinine concentrations were measured in additional groups (6 to 13 rats each) exposed to 3 days, 3 weeks, or 6 weeks of ETS and controls. Average air nicotine, carbon monoxide, and total particulate concentrations were 1103 micrograms/m3, 92 ppm, and 60 mg/m3 for the ETS-exposed rats. Infarct size (infarct mass/risk area x 100%) increased significantly in the ETS groups compared with the control groups in a dose-dependent manner (P = .023), with longer exposure associated with larger infarct size. Infarct size nearly doubled with 6 weeks of ETS exposure (61 +/- 5% versus 34 +/- 3% for control, mean +/- SEM). Plasma COHb, nicotine, and cotinine levels increased significantly in the ETS groups in a dose-dependent manner (all P < .001). CONCLUSIONS: Exposure to passive smoking increases myocardial infarct size in a rat model of ischemia and reperfusion. This increase of infarct size exhibited a dose-response relation. These results are consistent with epidemiological studies demonstrating that ETS increases the risk of heart death.

Animals↗
PubMed1994

Thrombolysis after acute myocardial infarction. Who should be added to inclusion criteria?

Thrombolytic therapy has been proven to be highly effective and safe in patients presenting with acute myocardial infarction. Its use may reduce mortality rates by as much as 50%. Accelerated administration of tissue plasminogen activator (Activase) combined with intravenous heparin shows particular success in reducing mortality rates, especially in patients with anterior infarcts. However, strict compliance to the classic inclusion criteria has limited the number of patients, excluding several groups who have been shown to benefit from thrombolysis: The elderly appear to benefit from early thrombolysis even more than do their younger counterparts. Patients with inferior myocardial infarction and bundle-branch blocks also benefit. Recent trials suggest that thrombolytic therapy can be cautiously extended to patients presenting late (up to 24 hours) after onset of symptoms. Certain patients with a history of cerebrovascular disease or recent surgery, patients with severe hypertension, and those having undergone cardiopulmonary resuscitation should not necessarily be excluded from consideration.

Anistreplase↗
PubMed1994

Adjuvants to thrombolysis after acute myocardial infarction. Does adding antiplatelet agents, antithrombotics, or angioplasty make a difference?

Thrombolytic therapy markedly reduces mortality and improves left ventricular function in patients with acute myocardial infarction. Improvement may be even more substantial with adjuvant therapy. Aspirin has proved to be effective adjuvant therapy to thrombolysis. Other antiplatelet agents that may be even more effective or have an additive effect with aspirin are being studied. The role of antithrombotic agents, especially heparin, as adjuvant therapy remains unclear. Immediate cardiac catheterization with angioplasty has been used as adjunct therapy, but its routine use is not recommended. Instead, elective angioplasty (cardiac catheterization, with revascularization as indicated) should be undertaken in patients with recurrent ischemia. Angioplasty as an alternative to thrombolysis may be advantageous in certain patients, such as those presenting in cardiogenic shock or with contraindications to thrombolysis. The role of primary angioplasty in other groups (eg, the elderly, those with anterior myocardial infarction) remains unclear, and further trials are necessary before it can be recommended over thrombolytic therapy. Equipment needed for angioplasty limits its practicality, whereas thrombolytic therapy can be administered at most US hospitals.

Angioplasty, Balloon, Coronary↗
PubMed1994

Nonglycoside inotropes in congestive heart failure. Are they beneficial or harmful?

Nonglycosidic adrenergic and nonadrenergic inotropic drugs improve systemic hemodynamics and left ventricular function in patients with severe congestive heart failure. As these beneficial effects are observed with short-term therapy, the use of these agents should be restricted to the treatment of acute heart failure. Long-term therapy with adrenergic agents as well as the phosphodiesterase inhibitors appears to enhance mortality in patients with chronic systolic heart failure. Potential indications for long-term therapy with nonglycosidic inotropic drugs include vesnarinone and ibopamine for selected patients with refractory heart failure or as pharmacologic bridges to cardiac transplantation.

Animals↗
PubMed1993

Successful excimer laser angioplasty following unsuccessful primary balloon angioplasty.

We report five patients where excimer laser coronary angioplasty facilitated successful balloon dilatation of heavily calcified lesions that could not be dilated by conventional angioplasty techniques alone. In each case, the lesion was crossed successfully with a guide wire. Conventional angioplasty failed because of inability to cross the lesion with a balloon (four lesions) or inability to dilate the lesion with balloon inflation (two lesions). These cases illustrate an indication for excimer laser coronary angioplasty as an adjunctive procedure in heavily calcified coronary stenoses.

Aged↗
PubMed1993

Assessment of perfused left ventricular mass in normal, ischemic, and reperfused myocardium by means of single-photon emission computed tomography of technetium-99m isonitrile.

To test the hypothesis that single-photon emission tomography of technetium (Tc) 99m hexakis 2-methoxyisobutyl isonitrile (Tc-MIBI) can accurately measure perfused left ventricular (LV) mass in nonischemic, ischemic, and reperfused myocardium, we acquired Tc-MIBI tomographic images in canines with normally perfused hearts (n = 33) after occlusion of the left anterior descending coronary artery (n = 15), after reperfusion (n = 13), and with subsequent second injection of Tc-MIBI (15 to 18 mCi; n = 12). In all ischemic studies the initial dose of Tc-MIBI (5 to 6 mCi) was injected after coronary artery occlusion but before reflow. Scintigraphic perfused LV mass was calculated from the total voxels demonstrating Tc-MIBI uptake x voxel volume (cm3) x specific gravity of myocardium (1.05 gm/cm3). After being imaged the animals were killed, the left ventricle was weighed, and the risk area was determined by dual perfusion with phthalocyanine blue dye and triphenyltetrazolium chloride (TTC). Perfused LV mass was defined as total LV mass minus the risk area mass. There was good correlation between scintigraphic and morphologic determinations of perfused left ventricular mass in nonischemic hearts (Tc-MIBI left ventricular distribution = 0.84 x left ventricular weight + .20.4, n = 33, r = 0.93, p = 0.0001) and ischemic hearts (Tc-MIBI left ventricular distribution = 0.51 x left ventricular weight + 37.9, n = 15, r = 0.83, p = 0.0001). In animals imaged both before and after reperfusion, scintigraphic determinations of the nonischemic region correlated closely (after-reflow Tc-MIBI distribution = 1.07 x before-reflow Tc-MIBI distribution--8.0, n = 13, r = 0.88, p = 0.0001), indicating that Tc-MIBI does not significantly redistribute into the ischemic zone after reperfusion. After injection of the second dose of Tc-MIBI in acutely reperfused canines, there was good correlation between the distribution mass of Tc-MIBI and the mass of viable myocardium by TTC staining (Tc-MIBI distribution = 0.61 x viable LV mass + 34.2, n = 12, r = 0.77, p = 0.0001). Furthermore, the apparent redistribution of myocardial Tc-MIBI from before and after second injection images correlated with the degree of myocardial salvage by histochemical staining (r = 0.72, p = 0.0082). In conclusion, single-photon emission computed tomography of Tc-MIBI can measure perfused LV mass accurately in both ischemic and nonischemic canine preparations.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Loss of myocardial protection after preconditioning correlates with the time course of glycogen recovery within the preconditioned segment.

BACKGROUND: Although previous investigators have demonstrated that myocardial preconditioning reduces infarct size, the mechanisms of cardioprotection associated with preconditioning are not completely understood. METHODS AND RESULTS: To test the hypothesis that preconditioning (four 5-minute episodes of ischemia each followed by 5 minutes of reperfusion) reduces infarct size by depleting cardiac glycogen stores and attenuating the degree of intracellular acidosis during subsequent prolonged left coronary artery occlusion, preconditioned and control rats were subjected to 45 minutes of left coronary artery occlusion and 120 minutes of reflow immediately after preconditioning (groups 1P and 1C, respectively) or after 30 minutes (groups 2P+30m and 2C), 1 hour (groups 3P+60m and 3C), or 6 hours (groups 4P+360m and 4C) of nonischemic recovery after preconditioning but before prolonged ischemia. In each group, cardiectomy was performed in selected rats immediately before prolonged ischemia for cardiac glycogen assay. In selected animals, 31P magnetic resonance spectroscopy was performed to monitor intracellular pH and measure high-energy phosphate levels during ischemia and reperfusion. Group 1P rats demonstrated marked glycogen depletion after preconditioning compared with controls (0.72 +/- 0.39 [n = 9] versus 5.67 +/- 1.73 [n = 12] mg glucose/g wet wt; p < 0.001 versus group 1C) that was associated with attenuation of intracellular acidosis during ischemia, as measured by 31P magnetic resonance spectroscopy (6.8 +/- 0.3 [n = 11] versus 6.2 +/- 0.3 [n = 9] pH units; p < 0.01), and marked infarct size reduction (0.3 +/- 0.6% [n = 7] versus 38.1 +/- 11.3% [n = 7], infarct size divided by risk area; p < 0.0001). During ischemia, there were no differences in myocardial ATP or phosphocreatine levels or in any hemodynamic determinant of myocardial oxygen demand between groups 1P and 1C. In preconditioned rats that were allowed to recover before ischemia (groups 2P+30m, 3P+60m, and 4P+360m), the time course of glycogen repletion paralleled the loss of protection from ischemic injury. CONCLUSIONS: Glycogen depletion and the attenuation of intracellular acidosis during ischemia appear to be important factors in delaying irreversible injury and reducing infarct size in this animal model of myocardial preconditioning.

Animals↗
PubMed1992

Cytoplasmic and mitochondrial tRNA nucleotidyltransferase activities are derived from the same gene in the yeast Saccharomyces cerevisiae.

ATP (CTP):tRNA-specific tRNA nucleotidyltransferase is an enzyme required for the synthesis of functional tRNAs in eukaryotic cells. Neither the tRNA genes in the nucleus nor in organelles encode the CCA end, so it must be added post-transcriptionally. The gene that codes for the enzyme that adds the CCA end to nuclear coded tRNAs in Saccharomyces cerevisiae has been isolated (Aebi, M., Kirchner, G., Chen, J.-Y., Vijayraghavan, U., Jacobson, A., Martin, N. C., and Abelson, J. (1990) J. Biol. Chem. 265, 16216-16220). We now demonstrate that there is a mitochondrial tRNA nucleotidyltransferase activity in yeast and that it is a matrix enzyme. A comparison of purified mitochondrial enzyme with its cytoplasmic counterpart revealed no differences. These results suggest that proteins responsible for this step in the maturation of tRNAs in the nucleus and mitochondria might be identical and coded by the same nuclear gene. Accumulation of shortened mitochondrial as well as cytoplasmic tRNAs in a strain with a temperature-sensitive tRNA nucleotidyltransferase is consistent with this hypothesis. Alteration of the wild type gene such that amino-terminal truncated proteins are produced leads to a defect in mitochondrial function and a decrease in mitochondrial nucleotidyltransferase activity. This provides a direct demonstration that one gene provides this enzyme activity for the biosynthesis of tRNAs in both the nuclear/cytoplasmic and mitochondrial compartments in yeast.

Amino Acid Sequence↗
PubMed1992

Magnetic resonance imaging demonstration of pharmacologic-induced myocardial vasodilatation using a macromolecular gadolinium contrast agent.

RATIONALE AND OBJECTIVES: Adenosine is a potent vasodilator used clinically in nuclear scintigraphy to assess coronary artery reserves. The potential to identify this vasodilating effect of adenosine using magnetic resonance imaging (MRI), which is superior in spatial resolution to nuclear scintigraphy, combined with a blood-pool MRI contrast agent, was investigated in normal rats. METHODS: Groups of Sprague-Dawley rats received successive infusions of either adenosine (3 mg/kg/minute; n = 7) or dipyridamole (negative control; up to 1.0 mg/kg/minute; n = 9), both before and after contrast enhancement, with a macromolecular blood-pool MRI contrast agent, albumin-gadolinium-DTPA35 (Gd-DTPA35) (4.0 mumol Gd per kilogram). Electrocardiographically (ECG) gated MRIs (2.0 Tesla), acquired serially before and after contrast enhancement, and with and without either adenosine or dipyridamole infusions, to monitor potential pharmacologic responses. RESULTS: During repeated infusions of adenosine, the postcontrast myocardial enhancement, reflecting blood volume, increased significantly (P < .05), up to 150%, compared with pre-adenosine enhancement. Infusions of dipyridamole, pharmacologically inactive in rats, produced no change in myocardial enhancement. CONCLUSIONS: The increased myocardial signal intensity observed during adenosine infusions after enhancement of the blood pool can be attributed to increased blood volume accompanying coronary vasodilatation. The method, which does not require a continuous infusion of contrast agent, has potential for the clinical evaluations of coronary artery reserves.

Adenosine↗
PubMed1992

Heat shock protein induction in rat hearts. A role for improved myocardial salvage after ischemia and reperfusion?

BACKGROUND: To test the hypothesis that the heat shock response is associated with improved myocardial salvage after myocardial ischemia and reperfusion, rats treated with prior whole-body hyperthermia and 24 hours of recovery (n = 26) or 20 minutes of ischemic pretreatment and 8 hours of recovery (n = 24) and control rats (n = 27, n = 24, for hyperthermic and ischemic pretreatment, respectively) were subjected to 35 minutes of left coronary artery (LCA) occlusion and 120 minutes of reperfusion. METHODS AND RESULTS: Although ventricular samples from rats subjected to either hyperthermia (n = 7) or ischemic pretreatment (n = 6) all showed induction of HSP72 (heat shock protein), Western blot analysis revealed significantly greater amounts of HSP72 in samples obtained from rats subjected to hyperthermia compared with those from rats subjected to ischemic pretreatment. Control rats (n = 7) showed no significant presence of myocardial HSP72. After 35 minutes of LCA occlusion and 2 hours of reperfusion, infarct size was significantly reduced in heat-shocked rats compared with controls (8.4 +/- 1.7%, n = 26 versus 15.5 +/- 1.9%, n = 27; p = 0.007; mean +/- SEM; infarct mass/left ventricular mass x 100). There were no significant differences in left ventricular (LV) systolic pressure, heart rate, LV dP/dt, or rate-pressure product between heat-shocked (n = 11) and control (n = 14) rats during the ischemic period. There were no differences in infarct size between ischemically pretreated and control rats subjected to 35 minutes of ischemia and reperfusion (9.7 +/- 2.1%, n = 23 versus 10.0 +/- 2.1, n = 24; p = NS). CONCLUSIONS: In this model of ischemia and reperfusion, prior heat shock was associated with significantly improved myocardial salvage after 35 minutes of LCA occlusion and reperfusion. This improved salvage was correlated with marked HSP72 induction and was independent of the hemodynamic determinants of myocardial oxygen supply and myocardial oxygen demand during the ischemic period. In contrast, mild HSP72 induction by ischemic pretreatment was not associated with improved myocardial salvage after myocardial ischemia and reperfusion. Thus, the absolute levels of HSP72 may be important in conferring protection from ischemic injury in this animal model.

Animals↗
PubMed1991

Noninvasive determination of left ventricular output and wall stress in volume overload and in myocardial disease by cine magnetic resonance imaging.

The current study used cine magnetic resonance imaging to determine the effect of increasing severity of valvular regurgitation on systolic wall stress and to demonstrate that wall stress was disproportionately increased in relation to the severity of regurgitation in patients with myocardial disease. A total of 39 patients with predominantly mitral (n = 22) or aortic (n = 17) regurgitation with (n = 13) and without (n = 26) myocardial disease and 10 normal volunteers were examined with cine magnetic resonance imaging (MRI) at 1.5 T. Left ventricular (LV) cardiac output (CO) and peak systolic (PS) wall stress (WS) and end-systolic (ES) WS were calculated from blood pressure recordings, carotid pulse tracings, and wall thickness (h) and diameter (D) measurements obtained from cine MRI. Patients were classified into three degrees of severity according to their LV regurgitant volume (RV). Myocardial disease was defined by an ejection fraction (EF) of less than 40%. Mean LV EF was 61 +/- 3% in normal volunteers, 64 +/- 3% in patients with regurgitation, and 25 +/- 2% in patients with myocardial disease. LV CO was directly related to RV in patients without myocardial disease, whereas it was disproportionately low in relation to RV in patients with myocardial disease. PS WS was significantly higher in severe mitral and/or aortic regurgitation compared with moderate, mild, and no mitral and/or aortic regurgitation. Compared with the degree of regurgitation, PS WS was disproportionately higher in patients with myocardial disease. Thus LV CO and WS rise progressively with increasing severity of regurgitation. Disproportionately high systolic WS relative to RV indicates the presence of myocardial disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Dipyridamole perfusion scintigraphy: the experience with its application in one hundred seventy patients with known or suspected unstable angina.

We evaluated the safety, accuracy, and potential clinical utility of intravenous dipyridamole perfusion scintigraphy with thallium-201 in 170 patients, 78 with suspected and 92 with known unstable angina. All had coronary angiography. Noncardiac side effects (26%), induced chest discomfort (44%), and ST segment changes (12%) were similar in the two groups. No significant arrhythmias occurred. Two patients had prolonged chest pain, both with extensive reversible image abnormalities and associated creatinine kinase-MB release. Both had elective bypass surgery. Twenty-eight patients had normal coronary arteries, and 35 had single-vessel disease. Scintigraphic per patient sensitivity and specificity were 91% and 79% with a per vessel sensitivity of 74% and a per vessel specificity of 78% without between-group differences. During a brief follow-up period, 62 patients with image abnormalities had coronary revascularization, and there were seven deaths without intergroup differences. In a similar patient group that did not have angiography, scintigraphic defects were less frequent and less extensive, revascularization was not performed, and subsequent deaths occurred less often. Dipyridamole perfusion scintigraphy is an accurate alternative to exercise testing in the evaluation of patients with unstable angina pectoris. Although not without risk, the method appears relatively safe and should be considered as a guide to diagnosis, and probably to prognosis and management.

Adult↗
PubMed1991

Myocardial protection with verapamil during ischaemia and reperfusion: dissociation between myocardial salvage and the degree of ATP depletion during ischaemia.

STUDY OBJECTIVE: The aim was to evaluate the protective effect of verapamil during myocardial ischaemia and reperfusion. DESIGN: In vivo phosphorus-31 (31P) magnetic resonance spectroscopy was performed on rats pretreated with verapamil (mg.kg-1 intraperitoneal) and controls during a 45 min left coronary artery occlusion and 60 min reperfusion. In separate groups of animals, haemodynamic measurements were taken at baseline, during ischaemia, and during reperfusion. Infarct size was determined by staining with triphenyltetrazolium chloride. EXPERIMENTAL MATERIAL: Female Sprague-Dawley rats were used (control group n = 25, experimental group n = 24). MEASUREMENTS AND MAIN RESULTS: Infarct size was significantly reduced in the verapamil group compared to controls: 9.9(SEM 2.3)%, n = 19 v 28.5(2.7)%, n = 19, p less than 0.001 (infarct % of left ventricular mass). Myocardial phosphocreatine and ATP levels were reduced to similar levels in both verapamil and control animals after 45 min ischaemia: 56.8(3.4)%, n = 10, v 61.4(1.8)%, n = 11 NS; 67.7(2.7)%, n = 10 v 69.7(2.9)%, n = 11, NS (% of baseline value). After 60 min reflow, there was significant recovery of phosphocreatine [91.1(4.2)% of baseline, p less than 0.05] and ATP [86.8(2.7)% of baseline, p less than 0.05] in the verapamil group, but no recovery of high energy phosphates in controls [66.3(2.8), NS; 69.6(2.7), NS]. The left ventricular systolic pressure, heart rate, rate-pressure product, and maximum rate of left ventricular pressure development were similar prior to ischaemia, and during ischaemia in both groups. There was an inverse correlation between infarct size and the degree of phosphocreatine recovery after 60 min of reperfusion (PCr recovery (%) = -0.99 x infarct size (%) + 101; r = 0.91; p less than 0.01; n = 14). Furthermore, in a separate group of animals (n = 9), there was a significant correlation between the size of the ischaemic area at risk and the degree of phosphocreatine decline after 15 min of coronary occlusion (PCr reduction (%) = 0.91 x risk area (%) + 5.6; r = 0.97; p less than 0.01). CONCLUSIONS: Pretreatment with verapamil extends the ischaemic time after which reperfusion results in myocardial salvage in this model of ischaemia and reperfusion. This protective effect is independent of the haemodynamic determinants of myocardial oxygen demand and the degree of ATP and phosphocreatine depletion during the ischaemic period. In this model of reversible ischaemia, 31P magnetic resonance spectroscopy is useful for quantitating both the size of the ischaemic region during coronary artery occlusion and infarct size after reperfusion.

Adenosine Triphosphate↗
PubMed1991

Normal and diffusely abnormal myocardium in humans: functional and metabolic characterization with P-31 MR spectroscopy and cine MR imaging.

The current study tested the concept that cine magnetic resonance (MR) imaging and phosphorus-31 MR spectroscopy might be used to provide a comprehensive evaluation of the functional and metabolic status of the myocardium in humans. Thirteen patients with congestive cardiomyopathy and eight healthy volunteers were imaged at 1.5 T with the one-dimensional chemical shift imaging technique for localization of P-31 MR spectroscopy and an electrocardiographically referenced gradient refocused sequence for imaging of the heart. Prominent peaks in the PDE and PME regions were observed in cardiomyopathic patients, but only the former peak was measured. The PCr/beta-ATP peak ratio was not significantly lower in cardiomyopathic patients compared with healthy subjects (1.51 +/- 0.08 vs 1.54 +/- 0.04). The ratios of PDE/PCr (0.80 +/- 0.07 vs 0.54 +/- 0.10) (P less than or equal to .01) and PDE/beta-ATP (1.19 +/- 0.10 vs 0.84 +/- 0.08) (P less than or equal to .05) were significantly higher in patients with dilated cardiomyopathy compared with healthy volunteers. Left ventricular systolic wall thickening was significantly lower and left ventricular peak and end-systolic wall stress and mass were significantly higher in cardiomyopathic patients compared with healthy volunteers. Thus, localized, gated P-31 MR spectroscopy combined with cine MR imaging allowed identification of both abnormal myocardial phosphate metabolism and abnormal ventricular function. While this study suggests that increased myocardial PDEs may be a marker for abnormal myocardium, the sensitivity and specificity of this marker need to be further evaluated.

Adenosine Triphosphate↗
PubMed1991

Polymorphous ventricular tachycardia associated with acute myocardial infarction.

BACKGROUND: During a 2.9-year period, 11 patients developed polymorphous ventricular tachycardia 1-13 days after acute anterior (seven patients) or inferior (four patients) myocardial infarction. None of the 11 patients had sinus bradycardia (mean heart rate, 90 +/- 23 beats/min), but three had a sinus pause immediately before the onset of polymorphous ventricular tachycardia. In all 11 patients, the QT interval and corrected QT interval (QTc) were normal or minimally prolonged (QT, 385 +/- 34 msec; QTc, 442 +/- 40 msec). None had significant hypokalemia (mean serum potassium concentration, 4.3 +/- 0.5 meq/l) or a grossly abnormal serum magnesium or calcium concentration (2.1 +/- 0.4 and 8.9 +/- 0.7 mg/dl, respectively). METHODS AND RESULTS: Immediately before the onset of polymorphous ventricular tachycardia, symptoms and/or electrocardiographic changes consistent with recurrent myocardial ischemia occurred in nine of 11 patients. One patient died before drug therapy could be initiated. Lidocaine was used in 10 patients and proved to be effective in only one. Intravenous procainamide was used in six patients: one improved, and five had recurrence of polymorphous ventricular tachycardia. Bretylium was used in five patients and was ineffective in all cases. Overdrive pacing was used in four patients and failed to suppress recurrent arrhythmias in all cases. Four patients with persistent polymorphous ventricular tachycardia unresponsive to lidocaine, procainamide, or bretylium responded to intravenous amiodarone. One patient with polymorphous ventricular tachycardia that was consistently preceded by ST segment elevation responded to intravenous nitroglycerin. Two patients with persistent polymorphous ventricular tachycardia and obvious recurrent ischemia unresponsive to pharmacological intervention responded to emergency coronary revascularization. A third patient who experienced recurrent angina and polymorphous tachycardia was initially stabilized with pharmacological therapy but subsequently underwent elective revascularization and has remained stable without antiarrhythmic therapy. CONCLUSIONS: Post-myocardial infarction polymorphous ventricular tachycardia is not consistently related to an abnormally long QT interval, sinus bradycardia, preceding sinus pauses, or electrolyte abnormalities. This arrhythmia has a variable response to class I antiarrhythmics but may be suppressed by intravenous amiodarone therapy. It is often associated with signs or symptoms of recurrent myocardial ischemia. Furthermore, coronary revascularization appears to be effective in preventing the recurrence of polymorphous ventricular tachycardia when associated with recurrent postinfarction angina.

Aged↗