Unsuitability of corrected QT dispersion as a marker for ventricular arrhythmias and cardiac sudden death after acute myocardial infarction.
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The present study investigated whether corrected QT (QTc) dispersion could play a role as a marker of ventricular arrhythmias and sudden cardiac death after acute myocardial infarction (MI). The study included 76 males and 24 females with a mean age of 60+/-11 years. Standard 12-lead ECGs were recorded during the recovery phase (15+/-9 days) after the onset of MI. The QTc was calculated according to Bazett's formula and QTc dispersion was calculated as the difference between the maximum and minimum QTc intervals. Patients were divided into 2 groups: 21 patients (group A) had a QTc dispersion of > or =80ms, and the other 79 patients (group B) had a QTc dispersion of <80ms in the recovery stage (15+/-9 days). Clinical, angiographical, and Holter monitoring data, and prognosis (mean follow-up period 29+/-18 months) were compared between these 2 groups. The frequencies of early coronary reperfusion and recanalization of infarct-related vessels during the recovery phase were significantly higher in group B than group A. The left ventricular ejection fraction was also higher in group B than group A (51+/-12 vs 43+/-12%, p=0.0029). There were no significant differences in the number of premature ventricular contractions, the percentage of patients with repetitive ventricular arrhythmias, or in the frequency of sudden cardiac death during the follow-up period between the 2 groups. In summary, QTc dispersion in the recovery stage is not a useful marker for ventricular arrhythmias or sudden cardiac death after acute MI, although increased QTc dispersion may correlate with an ineffective early coronary reperfusion and with the degree of depressed left ventricular function. (+info)
Torsades de pointes in a case of hypertrophic cardiomyopathy with special reference to the pathologic findings of the heart including the conduction system.
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A clinicopathologic study was performed in a 77-year-old female with hypertrophic cardiomyopathy who had experienced recurrent syncopal attacks due to Torsades de Pointes (TdP) following QT prolongation and atrioventricular block. She died suddenly two years later while eating dinner. Pathologic findings of the heart showed a dilated and hypertrophied left ventricle. The heart weighed 550 g. There were two foci of localized endocardial fibroelastosis (EFE) beneath the aortic valve, one with a size of 3.5 x 3.5 cm, and the other (2 x 1 cm) located on the upper ventricular septum. Histologic findings showed hypertrophy and disarray in the left ventricular myocardium. The conduction system using serial sectioning revealed remarkable bilateral bundle branch fibrosis and hypertrophied Purkinje fibers in the left bundle branch adjacent to the EFE on the ventricular septum. These findings were thought to be related to the occurrence of TdP. (+info)
Selective activation of the K(+)(ATP) channel is a mechanism by which sudden death is produced by low-energy chest-wall impact (Commotio cordis).
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BACKGROUND: Sudden death due to relatively innocent chest-wall impact has been described in young individuals (commotio cordis). In our previously reported swine model of commotio cordis, ventricular fibrillation (with T-wave strikes) and ST-segment elevation (with QRS strikes) were produced by 30-mph baseball impacts to the precordium. Because activation of the K(+)(ATP) channel has been implicated in the pathogenesis of ST elevation and ventricular fibrillation in myocardial ischemia, we hypothesized that this channel could be responsible for the electrophysiologic findings in our experimental model and in victims of commotio cordis. METHODS AND RESULTS: In the initial experiment, 6 juvenile swine were given 0.5 mg/kg IV glibenclamide, a selective inhibitor of the K(+)(ATP) channel, and chest impact was given on the QRS. The results of these strikes were compared with animals in which no glibenclamide was given. In the second phase, 20 swine were randomized to receive glibenclamide or a control vehicle (in a double-blind fashion), with chest impact delivered just before the T-wave peak. With QRS impacts, the maximal ST elevation was significantly less in those animals given glibenclamide (0.16+/-0.10 mV) than in controls (0.35+/-0.20 mV; P=0.004). With T-wave impacts, the animals that received glibenclamide had significantly fewer occurrences of ventricular fibrillation (1 episode in 27 impacts; 4%) than controls (6 episodes in 18 impacts; 33%; P=0.01). CONCLUSIONS: In this experimental model of commotio cordis, blockade of the K(+)(ATP) channel reduced the incidence of ventricular fibrillation and the magnitude of ST-segment elevation. Therefore, selective K(+)(ATP) channel activation may be a pivotal mechanism in sudden death resulting from low-energy chest-wall trauma in young people during sporting activities. (+info)
Abnormal cardiac repolarization and impulse initiation in German shepherd dogs with inherited ventricular arrhythmias and sudden death.
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OBJECTIVE: We tested the hypothesis that delayed afterdepolarization (DAD)-associated rhythms in German shepherd dogs with reduced anteroseptal left ventricular (LV) sympathetic innervation derive from abnormal beta-adrenergic receptor effector coupling. METHODS AND RESULTS: In anteroseptal LV midmyocardium of afflicted dogs, beta-receptor density was greater than that in normal dogs (P < .05), with affinity being equal in both groups. Basal and maximum isoproterenol (ISO) stimulated adenylyl cyclase activity of anteroseptal LV of afflicted dogs was greater than that in normal dogs (P < .05). Isolated anteroseptal M cell preparations of afflicted dogs studied with microelectrodes showed abnormal lengthening, rather than shortening of action potential duration in response to ISO, as well as a 61% incidence of 10(-7) mol/l ISO-induced triggered activity as compared to 12% in normals (P < .05). In contrast, there was no difference between afflicted and control dogs in triggered activity, beta-receptors or adenylyl cyclase activity in a normally innervated region of the ventricles. CONCLUSION: In this model there is an increase in beta-receptor density and beta-adrenergic stimulation of adenylyl cyclase and of triggered activity in anteroseptal myocardium but not in a normally innervated region of the heart. Hence, abnormal beta-adrenergic signal transduction appears associated with the neural abnormality identified in dogs with inherited VT. (+info)
A comparison of troponin T and troponin I as predictors of cardiac events in patients undergoing chronic dialysis at a Veteran's Hospital: a pilot study.
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OBJECTIVE: The purpose of this study was to prospectively evaluate the usefulness of the cardiac troponins as predictors of subsequent cardiac events in patients with chronic renal failure undergoing dialysis. BACKGROUND: Cardiac troponin T (cTnT) and I (cTnI) are cardiac markers that are specific for cardiac muscle. They are also excellent prognostic indicators for patients presenting with chest pain. Although cardiac disease is the leading cause of death in dialysis patients, standard methods to diagnose acute coronary syndromes in patients with renal failure are often misleading. METHODS: A six-month prospective study was done in a university-affiliated Veterans Hospital's dialysis clinic. Forty-nine patients undergoing chronic dialysis with no complaints of chest pain were followed for cardiac events occurring in the six months after cardiac troponin measurements. These included unstable angina, acute myocardial infarction and cardiac death. An additional 83 patients with renal failure but who were not undergoing dialysis were also examined. RESULTS: Within six months all three dialysis patients with elevated cTnI at entry into the study suffered an adverse complication (specificity and positive predictive value = 100%). Twenty-five patients had cTnT elevated at >0.10 ng/ml (53%). Patients with diabetes were more likely to have elevated troponin T levels (64% vs. 25%, p = 0.01). All six patients developing cardiac events within three months had elevations of cTnT >0.1 ng/ml (sensitivity = 100%). Whereas the specificity of cTnT was only 56% for a near-term cardiac event, the negative predictive value of cTnT using a cutoff of < or = 0.1 ng/ml was 100%. On restratifying patients using a cutoff value of cTnT of >0.2 ng/ml, only nine of 49 dialysis patients (18%) had elevated levels. In patients with renal failure not undergoing dialysis, only three of 83 (4%) had elevated troponin I or T. None of these patients suffered a cardiac event in the next six months. CONCLUSIONS: This prospective pilot study clearly delineates the troponins as important prognosticators in asymptomatic otherwise "stable" patients on chronic dialysis, especially those with concomitant diabetes mellitus. It also appears that troponins are more likely to be elevated in dialysis patients than other patients with renal failure not on dialysis. The above suggests that the combination of cTnI and cTnT might be very effective in elucidating cardiac risks of patients with renal failure undergoing chronic dialysis. (+info)
Prognostic value of MIBG imaging in idiopathic dilated cardiomyopathy.
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Alterations of cardiac sympathetic innervation are likely to contribute to fatal outcomes in patients with heart failure. These alterations can be evaluated noninvasively by 123I-metaiodoben-zylguanidine (MIBG) imaging. METHODS: The hypothesis that impaired cardiac sympathetic innervation, as assessed using MIBG imaging, is related to adverse outcomes was tested in 112 patients with heart failure resulting from idiopathic cardiomyopathy. Main inclusion criteria were New York Heart Association classes II-IV and radionuclide left ventricular ejection fraction (LVEF) < 40%. Patients were assessed for cardiac MIBG uptake, circulating norepinephrine concentration, LVEF, peak Vo2, x-ray cardiothoracic ratio, M-mode echographic end-diastolic diameter and right-sided heart catheterization parameters. RESULTS: During a mean follow-up of 27 +/- 20 mo, 19 patients had transplants, 25 died of cardiac death (8 sudden deaths), 2 died of noncardiac death and 66 survived without transplantation. The only independent predictors for mortality were low MIBG uptake (P < 0.001) and LVEF (P = 0.02) when using multivariate discriminant analysis. Moreover, MIBG uptake (P < 0.001) and circulating norepinephrine concentration (P = 0.001) were the only independent predictors for life duration when using multivariate life table analysis. CONCLUSION: Impaired cardiac adrenergic innervation as assessed by MIBG imaging is strongly related to mortality. MIBG imaging may help risk stratify patients with heart failure resulting from idiopathic dilated cardiomyopathy. (+info)
Autonomic modulation and QT interval dispersion in hypertensive subjects with anxiety.
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Anxiety is associated with an increased risk of sudden death. QT dispersion is a marker of cardiac repolarization instability and is seen in conditions of high risk of sudden death. The purpose of this study was to evaluate autonomic nervous system control and QT dispersion in hypertensive subjects with anxiety symptoms. In a recent preliminary study, we observed that hypertensive individuals reporting high scores on a self-assessment anxiety scale had more marked left ventricular hypertrophy. In 105 hypertensive subjects divided into 3 groups according to severity of anxiety, we evaluated autonomic control by short-term power spectral analysis of RR and arterial pressure variability at rest (baseline) and during sympathetic stress (tilt test), left ventricular mass index, and heart rate-corrected QT (QTc) dispersion. At baseline, hypertensive subjects with higher anxiety symptom scores had significantly lower high-frequency RR values expressed in absolute terms (P<0.05) and in normalized units (P<0.05) than their counterparts without anxiety symptoms. Hypertensive subjects with anxiety also had a higher mean left ventricular mass index (P<0.001) and greater QTc dispersion (P<0.001). Both indexes and high frequency (P<0.05) correlated with severity of anxiety. These findings suggest that anxiety is associated with autonomic imbalance. This condition could favor an increase in left ventricular mass. Myocardial hypertrophy alone or combined with neuroautonomic imbalance may lead to QT dispersion. (+info)
Mechanisms of progression in native coronary artery disease: role of healed plaque disruption.
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OBJECTIVE: To determine the role of healed plaque disruption in the generation of chronic high grade coronary stenosis. METHODS: Coronary arteries obtained at necropsy were perfuse fixed with formal saline for 24 hours at 100 mg Hg. The percentage lumen diameter stenosis was measured in each 3 mm segment containing a plaque, using the lumen size at the nearest histologically normal segment as the reference point. Each segment was prepared for histological examination and stained with Sirius red and immunohistochemistry for smooth muscle actin. Healed disruption was considered to be present when under polarised light there was a break in the yellow-white dense collagen of the cap filled in by more loosely arranged green collagen. Increased smooth muscle density in the green staining areas was required. Each section was read independently by two observers; any segment with discordant views was considered negative. MATERIAL: 31 men aged 51-69 dying suddenly of ischaemic heart disease. 39 coronary arteries were studied containing 256 separate plaques, after excluding coronary arteries with old total occlusions, an acute culprit thrombotic lesion, diffuse disease without normal arterial segments, and arteries related to old myocardial scars. RESULTS: 16 of 99 plaques causing < 20% diameter stenosis had prior disruption. In the 21-50% stenosis range 16 of 86 plaques showed healed disruption. Stenosis >/= 51% by diameter was present in 71 plaques, 52 of which showed a healed disruption pattern. The difference between stenosis < 50% and stenosis >/= 51% was significant by the chi(2) test (p < 0.001). CONCLUSIONS: Subclinical episodes of plaque disruption followed by healing are a stimulus to plaque growth that occurs suddenly and is a major factor in causing chronic high grade coronary stenosis. This mechanism would explain the phasic rather than linear progression of coronary disease observed in angiograms carried out annually in patients with chronic ischaemic heart disease. (+info)