Effect of balloon-induced acute ischaemia on P wave dispersion during percutaneous transluminal coronary angioplasty.

AIMS: P wave dispersion is a recent ECG marker that reflects discontinuous and inhomogeneous conduction of sinus impulses, which has been studied in a limited number of cardiac conditions. The aim of our study was to investigate the effects of angioplasty induced-ischaemia on atrial conduction abnormalities as estimated by P maximum and P dispersion. METHODS AND RESULTS: The study consisted of 67 consecutive patients (41 men, mean age 58 +/- 11 years) with 1-vessel coronary artery disease who underwent elective single vessel coronary angioplasty (left anterior descending (LAD) coronary artery in 28 patients, the right coronary artery (RCA) in 22 patients and the left circumflex coronary artery (LCx) in 17 patients. All patients underwent 12-lead surface ECG before the first inflation (baseline) and then 60 s after intra-coronary balloon inflation. The maximum P wave duration, the minimum P wave duration, and P wave dispersion (Pd=Pmax - Pmin) were calculated from 12-lead surface ECGs. Baseline P wave duration measurements were not significantly different among the patients with LAD, RCA and LCx coronary artery disease (P>0.05). P dispersion and P maximum were significantly higher during balloon occlusion compared with the baseline condition in all three types of coronary dilatation procedures. However, P minimum was not found to differ between baseline and during balloon occlusion (P>0.05). CONCLUSION: The prolongation of P wave dispersion may be a useful and simple additional marker for myocardial ischaemia.

Extent of coronary atherosclerosis and homocysteine affect endothelial markers.

The aim of the study was to evaluate the effects of the presence, extent, and clinical stability of coronary artery disease on endothelial function parameters, C-reactive protein and homocysteine levels. Fifty-eight patients with angiographically documented coronary artery disease and 25 patients with normal coronary arteries were evaluated for risk factors, plasma homocysteine, C-reactive protein, and soluble adhesion molecule levels. Vascular cell adhesion molecule-1 and sE-selectin were significantly higher in the group with coronary artery disease than in healthy subjects (p = 0.005 and p = 0.031, respectively). Patients with unstable angina had significantly higher C-reactive protein (p < 0.001), troponin I (p < 0.01), and leukocyte counts (p < 0.05) than those with stable angina. sE-selectin levels were correlated with the extent of coronary atherosclerosis (r = 0.444, p < 0.05), and plasma homocysteine levels were associated with vascular cell adhesion molecule-1 (r = 0.479, p < 0.05) in unstable cases. These results suggest that vascular cell adhesion molecule-1 and sE-selectin are useful for determining the presence of coronary atherosclerosis, whereas C-reactive protein, troponin 1, and leukocyte count are predictors of clinical stability.

What is the optimal evaluation time of the QT dispersion after acute myocardial infarction for the risk stratification?

The sequential changes of the corrected QT dispersion (QTcD) were studied in 136 patients 1 day to 30 days after a transmural acute myocardial infarction (AMI) to investigate the optimal measurement time of QT dispersion for risk stratification. The study group included 136 patients (89 men; mean age, 57+/-10 years) with transmural AMI who were treated with thrombolytics (Tr+ group, n = 73) or not (Tr- group, n = 63) and 65 healthy controls (43 men; mean age, 56+/-7 years). Fourteen patients in whom ventricular tachycardia (VT), ventricular fibrillation (VF), or sudden cardiac death developed during the 30-day period were also evaluated as major cardiac arrhythmia (MCA) group. ECGs were obtained for each patient on days 1, 3, 5, 10, 15, and 30 after AMI. QTc dispersion in patients with AMI (for every period of QTcD after MI) was significantly more prolonged than in normal controls (49.3+/-16.3 ms) (p<0.001). QTcD was significantly greater in patients without thrombolytics than in patients with thrombolytics for every period (days 1, 3, 5, 10, 15, and 30) of QTcD after MI (p<0.001). The mean of QTcD was significantly greater in patients with MCA than in patients without MCA group for every period (days 1, 3, 5, 10, 15, and 30) of QTcD after MI (p < 0.05). Maximal QTcD was seen on day 10 (p < 0.05 1st vs day 10 for each group) after myocardial infarction, and then reached a plateau for an each group. The ideal time to measure the QTD for risk stratification is at least 10 days after AMI.

The diagnostic value of 12-lead electrocardiogram in predicting infarct-related artery and right ventricular involvement in acute inferior myocardial infarction.

BACKGROUND: The aim of the present study was to investigate the predictive value of presentation and 24-hour electrocardiograms in defining the infarct-related artery (IRA), its lesion segment, and the right ventricular involvement in acute inferior myocardial infarction (MI). METHODS: One hundred forty-nine patients with acute inferior MI were included. Infarct-related artery, its lesion segment, and the validity of new ECG criteria for the diagnosis of right ventricular MI (RVMI) were investigated by means of criteria obtained from admission and 24- hour ECGs. RESULTS: The presence of ST-segment elevation in lead III > lead II criterion (Criterion 1) and ST-segment depression in lead I > lead aVL criterion (Criterion 2) from admission ECG defined the right coronary artery (RCA) as IRA with a sensitivity of 64% and a specificity of 100%. These two criteria also defined the proximal or mid lesions in RCA as culprit lesions (sensitivity of 99%, specificity of 96%). Absence of these two criteria indicated Cx as IRA with a sensitivity of 50% and a specificity of 97%. The depth of Q wave in lead III > lead II criterion (Criterion 3) had no value for discrimination of IRA, but the width of Q wave in lead III > lead II criterion (Criterion 4) supported the RCA to be IRA with a sensitivity of 60% and a specificity of 61% (Criteria 3 and 4 were obtained from 24-hour ECGs). The finding of Criterion 1 plus Criterion 5 (ST elevation in V(1) but no ST elevation in V2) on admission ECG had a sensitivity of 63% and a specificity of 99% in the diagnosis of RVMI. CONCLUSION: We concluded that 12-lead ECG is a cheap, easy, and readily obtainable diagnostic approach in discrimination of IRA and its culprit lesion segment. However, despite high specificity, due to moderate degree sensitivity, its value for the diagnosis of RVMI is questionable.

Acute anterior myocardial infarction following a mild nonpenetrating chest trauma--a case report.

Myocardial infarction in patients under age 45 years is a relatively unusual phenomenon; blunt chest trauma is one of the nonatherosclerotic mechanisms leading to acute myocardial infarction in young adults. The authors report a rare case of anterior myocardial infarction in a 22-year-old man following a mild nonpenetrating chest trauma whose left chest was elbowed during a soccer game.

Platelet and leukocyte deactivation after intracoronary stent placement in patients receiving combined antiplatelet therapy.

Activated platelets and leukocytes have been demonstrated to play a role in the development of stent thrombosis, and coronary angioplasty has been shown to result in activation of platelets, leukocytes, and endothelial cells. We aimed to evaluate the effects of intracoronary stent placement and aspirin plus ticlopidine treatment on platelets, leukocytes, and endothelial cells via observing the serial changes in the circulating soluble forms of adhesion molecules in 54 patients with coronary artery disease, who had elective coronary angioplasty and stent implantation for a single lesion of the left anterior descending artery. After stent placement, intravenous heparin infusion was administered only for 24 hours, and aspirin plus ticlopidine treatment was applied for 1 month. Venous blood samples were drawn before stent placement, and repeated 24 and 48 hours after the procedure. Patients were excluded if they had had recent cardiovascular events or any illness that might influence platelet, leukocyte, and endothelial cell function. The plasma level of sL-selectin was significantly decreased 48 hours after coronary stenting (636+/-110 ng/mL vs 567+/-93 ng/mL; P = 0.001, respectively). Likewise, the plasma level of sP-selectin was also decreased significantly 48 hours after the procedure (260+/-61 ng/mL vs 233+/-83 ng/mL, P = 0.01). The sE-selectin level was found to be significantly increased 24 hours (31+/-9 ng/mL vs 39+/-12 ng/mL, P = 0.0001) and 48hours(31+/-9 ng/mL vs 42+/-15 ng/mL, P = 0.001) after coronary stenting. The results of our study suggest that significant platelet and leukocyte deactivation take place in patients treated with combined antiplatelet therapy after stenting; endothelial cell activation also occurs during this treatment.

Increased plasma levels of soluble selectins in patients with unstable angina.

BACKGROUND: Inflammation plays an important role in the pathogenesis of unstable angina. Adhesion molecules, such as selectins, mediate the interactions between leukocytes, platelets and endothelial cells during inflammation and thrombogenesis. HYPOTHESIS: The purpose of this study was to determine whether soluble E-selectin, P-selectin and L-selectin levels are increased in patients with unstable angina (UA). METHODS: Soluble E-, P- and L-selectin levels were measured by enzyme-linked immunoassay in the peripheral blood of 23 patients with UA, 26 patients with stable angina (SA) and 15 control patients with angiographically normal coronary arteries. RESULTS: Soluble E-selectin levels were significantly higher in patients with UA (45+/-11 ng/ml) than in controls (30+/-8 ng/ml, P<0.001), or patients with SA (34+/-8 ng/ml, P=0.001). Similarly, plasma levels of P- and L-selectin were significantly higher in patients with UA (427+/-144 and 772+/-160 ng/ml, respectively) than in patients with SA (278+/-79 and 643+/-94 ng/ml, respectively, P<0.005 vs. UA for both), or control patients (189+/-43 and 601+/-126 ng/ml, respectively, P=0.001 vs. UA for both). CONCLUSIONS: Plasma levels of soluble selectins were increased in patients with UA compared with patients with SA or patients without angiographically visible coronary artery disease. Measurements of these adhesion molecules may be helpful as non-invasive markers of coronary plaque destabilization in UA.

Effects of stent coating on platelets and endothelial cells after intracoronary stent implantation.

BACKGROUND: Adhesion molecules are known to be important in the regulation of endothelial cell and platelet functions. Increased platelets P-selectin expression is a marker of stent thrombosis after uncoated stent placement. HYPOTHESIS: The aim of this study was to compare the effects of intracoronary placement of phosphorylcholine (PC)-coated, versus heparin-coated, versus uncoated stents on platelets and endothelial activity. METHODS: Thirty patients (age 55 +/- 10, 27 men) with significant proximal left anterior descending coronary artery stenoses were randomized to elective implantation of PC-coated, versus heparin-coated, versus uncoated stents. Following stent placement, intravenous heparin and aspirin plus ticlopidine were administered. Venous plasma soluble E-selectin, sP-selectin, and intercellular adhesion molecule-l levels were measured before the procedure and 24 and 48 h thereafter as markers of platelet and endothelial cell activation. Patients were excluded if they had a disease known to influence platelet and endothelial cell function. RESULTS: Plasma sP-selectin levels decreased significantly after implantation of PC- and heparin-coated stents (p = 0.04), but remained unchanged in patients randomized to uncoated stents. Plasma sE-selectin levels increased significantly after uncoated stent placement (p = 0.04) and remained unchanged after coated stent implantation. CONCLUSION: In patients treated with combined antiplatelet therapy, implantation of PC- and heparin-coated stents decreased platelet activity without activating endothelial cells, whereas placement of uncoated stents led to endothelial activation without changing platelet activity. These results suggest that PC-coated and heparin-coated stents may be advantageous in limiting thrombotic complications.

T wave alternans can decrease after coronary revascularization.

Clinical observations and animal experiments indicate that T wave alternans (TWA) is associated with an increased propensity for ventricular fibrillation, and thus it may be considered as a noninvasive marker of life-threatening ventricular arrhythmias. There is substantial evidence indicating that TWA is an intrinsic property of ischemic myocardium. This study was performed to determine the role of percutaneous transluminal coronary angioplasty (PTCA)-induced myocardial ischemia in the development of TWA and the effects of revascularization. The authors recorded bipolar X, Y, and Z leads of 111 consecutive patients (mean age: 56 years) undergoing PTCA before, during, and 24 hours after the procedure. T wave alternans signal was calculated in 97 patients (43 left anterior descending, 26 right coronary artery, and 28 circumflex or major obtuse margin branch) by fast Fourier transformation technique after signal processing. Twenty-four hours after the procedure, the mean and peak X, Y, and Z values for TWA had all been significantly reduced from baseline and during balloon inflation (p<0.01). The findings point out that induced ischemia could be a trigger for T wave alternans, and successful revascularization can reduce alternans.

QT dispersion as a predictor of arrhythmic events in patients with ankylosing spondylitis.

OBJECTIVE: The aim of the study was to evaluate QT dispersion (QTd), an indicator of repolarization heterogeneity, and its relation to ventricular arrhythmias in patients with ankylosing spondylitis (AS). METHODS: A full history, clinical examination, electrocardiograms and 24-h Holter monitoring were performed in 88 AS patients and 31 volunteers of similar age and sex. Groups were compared based on electrocardiographic abnormality, QTd, arrhythmias and heart blocks. RESULTS: QTd and corrected QTd (QTcd) were significantly greater in AS patients than controls (QTd, 52.8 +/- 15.1 vs 35.5 +/- 8.9 ms, P: < 0.0001; QTcd, 60.3 +/- 16.1 vs 39.4 +/- 10.7 ms, P: < 0.0001). The magnitudes of these parameters were associated with the duration of the disease (QTd, r = 0.56, P: < 0.01; QTcd, r = 0.60, P: < 0.001). The frequency of ventricular extrasystoles was found to be correlated with QTd (r = 0.35, P: < 0.01) and QTcd (r = 0.33, P: < 0. 01). CONCLUSION: Involvement of the heart may be seen in AS during the early clinical course of the disease. QTd may give clues about the presence of arrhythmias and can be used as a new technique for the evaluation of asymptomatic patients. Earlier detection of cardiac involvement could alter the prognosis of the patients.

Assessment of autonomic nervous system functions in patients with vitamin B12 deficiency by power spectral analysis of heart rate variability.

The purpose of this study was to test the autonomic nervous system function of patients with vitamin B12 deficiency (megaloblastic anemia) by measuring heart rate variability (HRV). The study population consisted of 17 vitamin B12 deficient patients and 15 age- and sex-matched normal volunteers. HRV was measured by power spectral analysis from which power of the low frequency (LF) peak (0.04-0.15 Hz), normalized units of the LF peak (LFNU), power of the high frequency (HF) peak (0.15-0.4 Hz), normalized units of the HF (HFNU), and ratio of power of LF to power of HF (LF:HF) were calculated. Vitamin B12 deficient patients had lower LF, LFNU, HF, HFNU, and LF:HF ratio than normal volunteers (P < 0.05). Decreases in sympathetic indices (LF and LFNU) were greater than those measured in parasympathetic indices (HF and HFNU). All HRV parameters correlated positively with the level of vitamin B12 (P < 0.001) and negatively with the duration of disease (P < 0.001). After vitamin B12 replacement the HRV parameters of patients and controls became comparable (P > 0.05). Our data suggest that autonomic sympathetic and parasympathetic nervous activities are decreased in patients with vitamin B12 deficiency, an abnormality that can be corrected by vitamin B12 replacement therapy.

P wave dispersion on 12-lead electrocardiography in patients with paroxysmal atrial fibrillation.

The prolongation of intraatrial and interatrial conduction time and the inhomogeneous propagation of sinus impulses have been shown in patients with atrial fibrillation. Recently P wave dispersion (PWD), which is believed to reflect inhomogeneous atrial conduction, has been proposed as being useful for the prediction of paroxysmal atrial fibrillation (PAF). Ninety consecutive patients (46 men, 44 women; aged 55 +/- 13 years) with a history of idiopathic PAF and 70 healthy subjects (42 men, 28 women; mean age 53 +/- 14 years) were studied. The P wave duration was calculated in all 12 leads of the surface ECG. The difference between the maximum and minimum P wave duration was calculated and this difference was defined as P wave dispersion (PWD = Pmax-Pmin). All patients and controls were also evaluated by echocardiography to measure the left atrial diameter and left ventricular ejection fraction (LVEF). There was no difference between patients and controls in gender (P = 0.26), age (P = 0.12), LVEF (66 +/- 4% vs 67 +/- 5%, P = 0.8) and left atrial diameter (36 +/- 4 mm vs 34 +/- 6 mm, P = 0.13). P maximum duration was found to be significantly higher in patients with a history of PAF (116 +/- 17 ms) than controls (101 +/- 11 ms, P < 0.001). P wave dispersion was also significantly higher in patients than in controls (44 +/- 15 ms vs 27 +/- 10 ms, P < 0.001). There was a weak correlation between age and P wave dispersion (r = 0.27, P < 0.001). A P maximum value of 106 ms separated patients with PAF from control subjects with a sensitivity of 83%, a specificity of 72%, and a positive predictive accuracy of 79%. A P wave dispersion value of 36 ms separated patients from control subjects with a sensitivity of 77%, a specificity of 82%, and a positive predictive accuracy of 85%. In conclusion, P maximum duration and P wave dispersion calculated on a standard surface ECG are simple ECG markers that could be used to identify the patients with idiopathic paroxysmal atrial fibrillation.

Circulating adhesion molecules in patients with stable coronary artery disease.

To evaluate platelet and endothelial function in patients with stable coronary artery disease (CAD), we investigated levels of the plasma-soluble (s) adhesion molecules E-selectin (sE-selectin), P-selectin (sP-selectin), and intercellular adhesion molecule-1 (sICAM-1) in 74 patients (mean age, 53 +/- 8 years) with angiographically documented coronary artery disease. Levels were compared to 27 matched healthy control subjects. Patients were excluded if they had recent cardiovascular events or any illness that might influence platelet and endothelial cell function. Concentrations of sP-selectin were significantly higher in patients with stable CAD (276 +/- 61 ng/mL) compared with control subjects (188 +/- 32 ng/mL) (P = .0001), whereas sE-selectin and sICAM-1 levels were similar between the 2 groups. Pooling both groups showed that sICAM-1 correlated weakly with triglycerides (r = 0.240, P = .01) and sP-selectin correlated weakly with low-density lipoprotein cholesterol (r = 0.204, P = .04). Although plasma sICAM-1 concentrations were significantly increased in hypercholesterolemic patients compared with those of normocholesterolemic patients (P = .04), sP-selectin and sE-selectin levels were similar between the 2 groups. In conclusion, significantly increased sP-selectin levels, indicating platelet activation, were found in patients with stable CAD. No other sign of endothelial cell activation in these patients could be detected. Moreover, sP-selectin levels seem to reflect the activation of platelets rather than of endothelial cells.

P wave dispersion in hypertensive patients with paroxysmal atrial fibrillation.

It is important to assess the risk of developing paroxysmal atrial fibrillation (PAF) in hypertensive patients since hypertension is a common disorder predisposing to PAF. We sought to determine if patients with hypertension at risk of PAF can be identified while in sinus rhythm by measurements of P wave dispersion. Twelve-lead surface electrocardiograms were recorded in 44 hypertensive patients with history of PAF (group I, mean age = 60) and in 50 hypertensive patients without history of AF (group II, mean age = 57). The maximum P wave duration, the minimum P wave duration, and P wave dispersion (Pd = Pmax - Pmin) were calculated from 12-lead surface ECGs. Left atrial dimension (LAD) and left ventricular ejection fraction (LVEF) were measured by echocardiography. P wave dispersion was significantly greater in group I than group II (50 +/- 12 vs 38 +/- 8 ms, P = 0.001). P minimum (75 +/- 13 vs 87 +/- 11 ms, P = 0.001) and LVEF (0.63 +/- 0.05 vs 0.67 +/- 0.04, P = 0.03) were significantly lower in group I than group II. However P maximum and LAD were not significantly different in group I than group II (P > 0.05). In univariate analysis, P minimum, P wave dispersion, and LVEF were significant predictors of PAF, whereas only P wave dispersion remained a significant independent predictor of PAF in a multivariate analysis. Measurement of P wave dispersion in sinus rhythm may be a useful noninvasive clinical tool to identify patients with hypertension at risk of developing atrial electrical instability and atrial fibrillation.

QT dispersion plus ST-segment depression: a new predictor of restenosis after successful percutaneous transluminal coronary angioplasty.

BACKGROUND: ST-segment depression during exercise testing is frequently observed in the absence of restenosis after percutaneous transluminal coronary angioplasty (PTCA). HYPOTHESIS: With the goal of improving the prediction of restenosis after PTCA, we evaluated the usefulness of ST-segment depression plus QT dispersion (QTd = QTmax - QTmin) during treadmill stress test. METHODS AND RESULTS: Fifty-six patients (37 men, 19 women, mean age 51 +/- 14 years) were evaluated with treadmill exercise testing and coronary angiography 7 +/- 5 months after PTCA. Treadmill test was positive in 30 patients and negative in 26 patients. At coronary angiography, restenosis was present in 16 patients with positive exercise electrocardiogram (ECG) and in 6 patients with negative exercise ECG. Fourteen patients with a positive stress test did not have restenosis. There was no difference in QTd values between groups at baseline (p > 0.05). Exercise QTd was 63 +/- 9 ms in patients with positive exercise test, 54 +/- 18 ms in patients with negative exercise test (p = 0.003), 71 +/- 13 ms in patients with restenosis, and 53 +/- 17 ms in patients without restenosis (p = 0.001). ST-segment depression during the stress test determined restenosis with a sensitivity of 80% and a specificity of 58%. Sensitivity and specificity of QTd of > or = 60 ms for prediction of restenosis were 83 and 61%, respectively. When QTd of > or = 60 ms was added to ST-segment depression as a condition for positive test, the sensitivity and specificity increased to 91 and 78%, respectively. QT dispersion plus ST-segment depression had higher sensitivity and specificity than either QTd or ST-segment depression alone (p < 0.05). CONCLUSION: The addition of QTd to ST-segment depression during exercise test improves the diagnostic value and can be used as a noninvasive tool in the diagnosis of restenosis after PTCA.

Circadian variations of QTc dispersion: is it a clue to morning increase of sudden cardiac death?

BACKGROUND: Several studies related to cardiac events including sudden death have shown a peak incidence in the early morning hours. It has also been known that acute ischemia is a potent stimulus to increased dispersion of repolarization and development of malignant arrhythmias. HYPOTHESIS: The purpose of the present study was to investigate diurnal variations of corrected QT dispersion (QTcD) in patients with coronary artery disease (CAD) (Group 1) compared with controls with normal coronary angiograms (Group 2). METHODS: We investigated a total of 110 patients who had been referred for coronary angiography, of whom 62 (42 men, 20 women; age 55 +/- 7 years) had double- or triple-vessel disease, and of whom 48 (31 men, 17 women; age 54 +/- 9 years) had normal coronary angiograms. QTcD measurements were calculated from a 12-lead resting electrocardiogram (ECG) during sinus rhythm. These ECGs were obtained for each patient in the morning, at noon, in the evening, and at night on the day after performance of coronary angiography. QTcD was significantly greater in patients with abnormal coronary angiograms (Group 1) than in patients with angiographically documented normal coronary arteries (Group 2). This difference appeared to be more prominent in the morning hours (p < 0.001) than at other times. QTcD in the evening and night hours was not statistically different (p > 0.05) between both groups. We also compared intragroup QTcD values: QTcD values were significantly increased in the morning hours and were more prominent in Group 1 than in Group 2. CONCLUSIONS: Our data suggest that QTcD has a circadian variation with an increase in the morning hours, especially in patients with coronary artery disease. This finding was thought to be an explanation for the role played by sympathetic nervous system in the occurrence of acute cardiac events and sudden death during these hours.

Effect of balloon inflation-induced acute ischemia on QT dispersion during percutaneous transluminal coronary angioplasty.

BACKGROUND: QT dispersion (QTd = QTmax-QTmin) measured as interlead variability of QT interval reflects the spatial inhomogeneity of ventricular repolarization times, and increased QTd may provide a substrate for malignant ventricular arrhythmias. Ischemia is associated with regional abnormalities of conduction and repolarization. HYPOTHESIS: This study aimed to investigate the effect of acute ischemia on QTd during successful percutaneous transluminal coronary angioplasty (PTCA). METHODS: Forty-three patients (10 women, 33 men, mean age 56 years) were enrolled in the study. Electrocardiogram (ECG) recordings were taken before PTCA and during balloon inflation period. QT maximum (QTmax), QT minimum (QTmin), and QTd (QTmax-QTmin) values were calculated from the surface ECG. RESULTS: There was no difference among QTmax values (p = 0.6). Mean QTmin during balloon inflation was lower than before PTCA (368 +/- 45 vs. 380 +/- 41 ms, p = 0.002). The difference between QTd values before and during balloon inflation was statistically important (65 +/- 9 vs. 76 +/- 10 ms, p = 0.001). This difference is caused by a decrease in QTmin during balloon inflation. CONCLUSION: Acute reversible myocardial ischemia induced by balloon inflation causes an increase in QTd value, and this increment is the result of a decrease in QTmin interval. Therefore, QTd may be a marker of reversible myocardial ischemia.

Is there any association between dissection after successful percutaneous transluminal coronary angioplasty and late restenosis? An angiographic study.

Restenosis continues to be the most important limitation of percutaneous transluminal coronary angioplasty (PTCA). Many clinical, angiographic, and procedural variables are thought to be related to the development of restenosis. This study was aimed at investigating the effects of no dissection, minor dissections, and major dissections on the long-term outcome of lesions after successful PTCA. The study group comprised 91 patients with 100 lesions who underwent successful PTCA and in whom follow-up coronary angiography was performed at 8.8 +/- 7.2 (two to twenty-three) months after dilation. Dissections were classified according to the National Heart, Lung, and Blood Institute criteria. Restenosis was defined as more than 50% stenosis at follow-up angiography. Restenosis rates were found to be 22% in the no-dissection group (10 restenoses in 46 patients), 27% in the minor dissection group (11 restenoses in 40 patients), and 36% in the major dissection group (5 restenoses in 14 patients). The authors applied corrected Yates Chi-square test and no difference was observed in the restenosis rate between the group without any dissections and that with minor dissections (P > 0.05). However, a statistically significant difference was observed in the restenosis rate between the major dissection group and the other two groups (P < 0.05). The authors conclude that the occurrence of major dissections after successful PTCA may adversely affect the long-term outcome and may increase the restenosis rate.