Investigation of the most effective provocation test for patients with coronary spastic angina: usefulness of accelerated exercise following hyperventilation.
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This study sought to compare the clinical usefulness of the hyperventilation plus cold stress test or the hyperventilation combined with accelerated exercise test with other single tests in patients with coronary spastic angina. The study examined 24 patients (23 men, mean age 66 years) with angiographically confirmed coronary spastic angina and less than 50% stenosis. Moreover, none had spontaneous ST segment elevation before the study. Under no medication for at least 24 h prior, 4 procedures were performed from 09.00 h to 11.00 h: (i) a hyperventilation test for 5 min (HV(5)); (ii) HV(5) combined with a cold stress test for the last 2 min (HV(5)+CS(2)); (iii) a treadmill exercise test based on Bruce's protocol (TM(3)); and (iv) a treadmill exercise test accelerated at 1 min intervals according to Bruce's protocol immediately after HV(5) (HV(5)+TM(1)). The rate of appearance of chest pain and ischemia-induced ECG changes due to HV(5)+TM(1) were significantly higher than the other 3 tests. HV(5)+CS(2) was not superior to HV(5) alone. The incidence of provoked ST segment elevation due to HV(5)+TM(1) was higher than with the other 3 procedures. Thus, in patients with coronary spastic angina, no spontaneous ST segment elevation and near normal coronary arteries, HV(5)+CS(2) was no more useful than HV(5) alone. It is recommended that the newly designed HV(5)+TM(1) combination test be used for documenting evidence of ischemia in patients with coronary spastic angina, low disease activity and near normal coronary arteries. (+info)
Determinants of exercise-induced ST-segment displacement in the aVL lead in patients with known or suspected coronary artery disease.
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Although the aVL lead in exercise electrocardiography is reported to be helpful in identifying a significant narrowing of the left anterior descending coronary artery (LAD), its role in exercise testing has not been fully evaluated. Accordingly, 821 patients who underwent both standard exercise testing and coronary angiography were evaluated. In patients with aVL lead ST elevation, the incidence of a significant narrowing of the LAD (124/165 vs 348/656; p<0.001) was higher than in those without. Multiple logistic regression analysis revealed that the 2 most important variables that correlated with aVL lead ST elevation were a greater number of leads with ST depression in the inferior leads and a smaller amplitude of R wave in the aVL lead. In contrast, variables correlating with aVL lead ST depression in the majority of cases were a greater number of leads with ST depression in all leads and the presence of inferior lead ST elevation. The results of this study indicate that although aVL lead ST elevation could be a marker for LAD narrowing, more important factors such as inferior lead ST-segment depression and the R-wave amplitude of the aVL lead should be taken into consideration. In contrast, ST depression in the aVL lead mostly represents exercise-induced myocardial ischemia of greater extent and severity. (+info)
Rapid progression of cardiomyopathy in mitochondrial diabetes.
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Cardiac involvement and its clinical course in a diabetic patient with a mitochondrial tRNA(Leu)(UUR) mutation at position 3243 is reported in a 54-year-old man with no history of hypertension. At age 46, an electrocardiogram showed just T wave abnormalities. At age 49, it fulfilled SV1 + RV5 or 6>35 mm with strain pattern. At age 52, echocardiography revealed definite left ventricular (LV) hypertrophy, and abnormally increased mitochondria were shown in biopsied endomyocardial specimens. He was diagnosed as having developed hypertrophic cardiomyopathy associated with the mutation. However, at age 54, SV1 and RV5,6 voltages were decreased, and echocardiography showed diffuse decreased LV wall motion and LV dilatation. Because he had mitochondrial diabetes, the patient's heart rapidly developed hypertrophic cardiomyopathy, and then it seemed to be changing to a dilated LV with systolic dysfunction. Rapid progression of cardiomyopathy can occur in mitochondrial diabetes. (+info)
A patient with hypertrophic cardiomyopathy accompanied by right ventricular dilation of unknown cause.
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Hypertrophic cardiomyopathy (HCM) is a disease characterized by an unknown cause of hypertrophy in the left or right ventricle. The dilated phase of HCM shows disease conditions resembling dilated cardiomyopathy, such as ventricular dilation, thin ventricular wall, and reduction of the ejection fraction. A patient presented with left ventricular concentric hypertrophy accompanied by right ventricular dilatation of unknown cause. Right ventricular endomyocardial biopsy specimens showed characteristic myocardial disarray. Therefore, there is the possibility that the patient had right and left ventricular HCM in the process toward the dilated phase, in which dilatation first occurred in the right ventricle. (+info)
Detection of abnormal high-frequency components in the QRS complex by the wavelet transform in patients with idiopathic dilated cardiomyopathy.
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In order to investigate whether increased fine, fractionated signals within the QRS complex can detect arrhythmogenic substrates and how these fine signals link with ventricular mechanical dysfunction, wavelet analysis was performed on averaged QRS complexes obtained from the left precordial lead in 26 patients with idiopatic dilated cardiomyopathy (IDCM) and in 12 normal subjects. The number of local maxima and the duration of the wavelet transform were significantly greater in patients with IDCM than in normal subjects; the number at 100 Hz was 8.8+/-3.1 vs 6.0+/-1.1 (p<0.01), and the duration at 100Hz was 93+/-15 vs 75+/-7ms (p<0.01). Both of these indices were greater in the patients with than in those without late potentials, repetitive ventricular premature beats or cardiac death. In addition, significant inverse curvilinear relationships were observed between the left ventricular ejection fraction and both the number of local maxima and the duration of the wavelet transform. In conclusion, fine fragmented signals in the QRS complex detected by wavelet analysis would be an important marker for potentially arrhythmogenic substrates and seemed to progress in parallel with left ventricular mechanical dysfunction in IDCM. (+info)
Detecting myocardial salvage after primary PTCA: early myocardial contrast echocardiography versus delayed sestamibi perfusion imaging.
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The extent of myocardial salvage after primary percutaneous transluminal coronary angioplasty (PTCA) in acute myocardial infarction (AMI) is variable and cannot be predicted on the basis of either vessel patency or early regional wall motion assessment. The aim of this study was to evaluate the reliability of microvascular integrity, as shown by myocardial contrast echocardiography (MCE), as an indicator of tissue salvage and a predictor of late functional recovery, and to compare MCE with the quantification of tracer activity in sestamibi perfusion imaging. METHODS: Twenty-six patients with AMI who received successful treatment with primary PTCA were examined with MCE during cardiac catheterization immediately before and after vessel recanalization. Myocardial contrast effect was scored as 0 (absent), 0.5 (partial) or 1 (normal). Wall motion was assessed by two-dimensional echocardiography on admission and 1 mo later with a 16-segment model and 4-point score. Resting sestamibi SPECT was collected within 1 wk after AMI. The risk area was defined by MCE as the sum of the segments with no perfusion (score 0) before PTCA. Myocardial viability was defined by MCE as an increase in contrast score in the same segments after PTCA and by sestamibi SPECT as a preserved tracer activity (>60% of peak activity). The functional recovery after 1 mo detected by two-dimensional echocardiography was the reference standard for viability. RESULTS: A total of 50 segments showed perfusion defects before PTCA (risk area). Immediately after PTCA, the MCE score increased in 44 of 50 segments, whereas sestamibi SPECT showed preserved activity in 22 of 50 segments. After 1 mo, the wall motion score decreased in 22 of 50 segments (viable segments) and was unchanged in the remaining 28 segments. Thus, MCE showed a sensitivity of 91% and a specificity of 14% in detecting viable myocardium, whereas sestamibi SPECT showed a lower sensitivity (68%) but a significantly higher specificity (75%; P < 0.00001). The positive predictive values were 45% and 68% for MCE and SPECT (P < 0.005), respectively, and the negative predictive values were 67% and 71%, respectively. On a patient basis, SPECT was more specific (79% versus 21%; P < 0.01) and showed a higher overall predictive accuracy (88% versus 50%; P < 0.01) than MCE. CONCLUSION: The demonstration of microvascular integrity by MCE performed immediately after primary PTCA has a limited diagnostic value in predicting salvaged myocardium. Conversely, tracer activity quantification in resting sestamibi SPECT performed in a later stage is confirmed to be a reliable approach for recognizing myocardial stunning and predicting functional recovery. (+info)
QT dispersion as an attribute of T-loop morphology.
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BACKGROUND: The suggestion that increased QT dispersion (QTD) is due to increased differences in local action potential durations within the myocardium is wanting. An alternative explanation was sought by relating QTD to vectorcardiographic T-loop morphology. METHODS AND RESULTS: The T loop is characterized by its amplitude and width (defined as the spatial angle between the mean vectors of the first and second halves of the loop). We reasoned that small, wide ("pathological") T loops produce larger QTD than large, narrow ("normal") loops. To quantify the relationship between QTD and T-loop morphology, we used a program for automated analysis of ECGs and a database of 1220 standard simultaneous 12-lead ECGs. For each ECG, QT durations, QTD, and T-loop parameters were computed. T-loop amplitude and width were dichotomized, with 250 microV (small versus large amplitudes) and 30 degrees (narrow versus wide loops) taken as thresholds. Over all 1220 ECGs, QTDs were smallest for large, narrow T loops (54.2+/-27.1 ms) and largest for small, wide loops (69. 5+/-33.5 ms; P<0.001). CONCLUSIONS: QTD is an attribute of T-loop morphology, as expressed by T-loop amplitude and width. (+info)
Cellular and ionic basis for T-wave alternans under long-QT conditions.
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BACKGROUND: T-wave alternans (TWA), an ECG phenomenon characterized by beat-to-beat alternation of the morphology, amplitude, and/or polarity of the T wave, is commonly observed in the acquired and congenital long-QT syndromes (LQTS). This study examines the cellular and ionic basis for TWA induced by rapid pacing under conditions mimicking the LQT3 form of the congenital LQTS in an arterially perfused canine left ventricular wedge preparation. METHODS AND RESULTS: Transmembrane action potentials from epicardial, M, and endocardial cells and 6 to 8 intramural unipolar electrograms were simultaneously recorded together with a transmural ECG and isometric tension development. In the presence of sea anemone toxin (ATX-II; 20 nmol/L), an increase in pacing rate (from a cycle length [CL] of 500 to 400 to 250 ms) produced a wide spectrum of T-wave and mechanical alternans. Acceleration to CLs of 400 to 300 ms produced mild to moderate TWA principally due to beat-to-beat alternation of repolarization of cells in the M region. Transmural dispersion of repolarization during alternans was exaggerated during alternate beats. Acceleration to CLs of 300 to 250 ms caused more pronounced beat-to-beat alternation of action potential duration (APD) of the M cell, resulting in a reversal of repolarization sequence across the ventricular wall, leading to alternation in the polarity of the T wave. The peak of the negative T waves coincided with repolarization of the M region, whereas the end of the negative T wave coincided with the repolarization of epicardium. In almost all cases, electrical alternans was concordant with mechanical alternans. Torsade de pointes occurred after an abrupt acceleration of CL, which was associated with marked TWA. Both ryanodine and low [Ca2+]o completely suppressed alternans of the T wave, APD, and contraction, suggesting a critical role for intracellular Ca2+ cycling in the maintenance of TWA. CONCLUSIONS: Our results suggest that TWA observed at rapid rates under long-QT conditions is largely the result of alternation of the M-cell APD, leading to exaggeration of transmural dispersion of repolarization during alternate beats, and thus the potential for development of torsade de pointes. Our data also suggest that unlike transient forms of TWA that damp out quickly and depend on electrical restitution factors, the steady-state electrical and mechanical alternans demonstrated in this study appears to be largely the result of beat-to-beat alternans of [Ca2+]i. (+info)