BACKGROUND AND PURPOSE: Chronic liver disease frequently includes cognitive and movement disorders, suggesting an alteration of the striatum. With the exception of hyperintensities evident on T1-weighted images indicative of Mn deposition, radiographic findings of the BG are nonspecific. Volumetric and morphometric analysis of DGM is limited. Whether DGM undergoes degeneration and whether this change is associated with pallidal hyperintensity and cognitive performance are currently unknown in patients with cirrhosis. MATERIALS AND METHODS: The DGM volumes of 28 patients with chronic cirrhosis and 28 control patients were compared. Using 3D high-resolution MR images, the volume and shape of each structure were automatically analyzed by the FSL. Correlations between the DGM volume and other clinical variables, including the pallidal signal intensity, were assessed by multiple regression analysis. RESULTS: Patients with Child B and Child C liver disease had significantly smaller bilateral putaminal volumes than control patients, and patients with Child C also demonstrated smaller left caudate nucleus and left amygdala volumes than control patients. Pallidal hyperintensity correlated with smaller striatum volume, which was linearly related to worse cognitive performance. The nonuniform distributed shape abnormalities in the striatum further support the ascending spiral interconnecting theory of the striatum. CONCLUSIONS: These findings strongly suggest lower DGM volume develops according to the severity of the liver cirrhosis. The Mn deposition might contribute the striatum deficit. These findings support the value of additional psychomotor research associated with liver cirrhosis.

Objective. A kidney transplant is a suitable surgical management for end-stage renal disease patients; however, posttransplantation malignancy is an unwanted outcome. In Taiwan, hepatocellular carcinoma (HCC) is a major malignancy not only among the general population but also in the post-kidney transplant group. Therefore, regular imaging studies for posttransplantation follow-up are necessary. We examined the imaging characteristics and the efficacy of radiologic diagnostic criteria and the American Joint Committee on Cancer (AJCC) staging system in post-kidney transplantation HCC.Patients and Methods. We retrospectively reviewed 15 patients with post-transplantation HCC among 554 hospital-based kidney transplant recipients. From 1988 to 2008 we analyzed the patient profiles, imaging studies, histopathologic diagnosis, treatment methods, and outcomes. The 6th-edition AJCC radiologic staging system was applied for validation in this study.Results. Using the AJCC staging system, all 15 patients with histopathologically confirmed HCC were enrolled as stage I (n = 7), stage II (n = 2), stage IIIA (n = 5), or stage IV (n = I) cases. The 5-year survival rates were 71.4% in stage I, 50% in stage II, 20% in stage IIIA, and 0% in stage IV. Over one-half of post-kidney transplantation HCC were sized 2.5-6.0 cm in diameter with mixed echogenicity. The positive diagnostic rate for adiologic criteria was 83.3%.Conclusions. The AJCC staging system and the radiologic diagnostic criteria were validated in post-kidney transplantation HCC. Surgical resection and transcatheter arterial embolization for early-stage HCC in kidney transplant recipients showed satisfactory outcomes. A noncirrhotic liver in a kidney transplant recipient makes surgical resection the treatment of choice because of the better prognosis.

STUDY OBJECTIVES Atrioesophageal fistulas have been reported to be a lethal complication following catheter ablation of atrial fibrillation (AF). The purpose of this study was to investigate the relationship between the esophagus and posterior left atrium (LA) and provide the anatomic information necessary to minimize the risk of esophageal injury during AF ablation. METHODS AND RESULTS Forty-eight patients (43 men; mean +/- SD age, 59 +/- 12 years) with drug-refractory paroxysmal AF and 32 control subjects (26 men; mean age, 60 +/- 9 years) were included. All underwent a CT scan for delineation of the relationship between the esophagus and posterior LA. In the paroxysmal AF group, two major types of esophageal routes were demonstrated. Type 1 routes were found in 42 patients with the lower portion of esophagus close to the ostium of the left inferior pulmonary vein (LIPV), including three subtypes of courses according to the proximity to the left superior pulmonary vein (PV) and LIPV. Type 2 routes were found in six patients with the lower portion of esophagus close to the ostium of the right inferior pulmonary vein (RIPV), including three subtypes of courses according to the proximity to the right superior PV and RIPVs. The mean shortest distance of the esophagus to the four individual PVs significantly differed between type 1 and type 2: 28.4 +/- 6.1 mm vs 10.5 +/- 5.7 mm (to the right superior), 19.6 +/- 7.0 mm vs 3.7 +/- 3.4 mm (to the right inferior), 10.1 +/- 3.4 mm vs 22.8 +/- 4.2 mm (to the left superior), and 2.8 +/- 2.5 mm vs 18.7 +/- 5.2 mm (to the left inferior), respectively (p < 0.001 for all). Contact of the esophagus and middle part of posterior LA was observed in each patient. However, direct contact of the aorta with the posterior LA wall was more frequent in type 2 than in type 1 (p = 0.001). The clinical characteristics, type of esophageal routes, distance from the esophagus to the four PVs, and diameter of the thoracic cage, LA, and aorta in the control group were similar to those in the AF group (p > 0.05 for all). CONCLUSION Although the anatomic relationship between the esophagus and LA posterior wall varied widely, two major patterns of esophageal routes could be depicted. This information is important for deciding the location of the ablation lesions around the PV ostia and LA and for avoiding the potential risk of esophageal injury.

Angiotensin-converting enzyme (ACE) inhibition has been shown to improve clinical myocardial ischemia in patients with syndrome X (angina pectoris, positive treadmill exercise test, normal coronary angiograms, and no evidence of coronary spasm). This study was conducted to investigate the effects of long-term ACE inhibitors on endothelial nitric oxide (NO) metabolism and coronary microvascular function in patients with syndrome X. After a 2-week washout period, 20 patients with syndrome X were randomized to receive either enalapril, an ACE inhibitor, 5 mg twice daily (n = 10) or placebo (n = 10) in a double-blind design for 8 weeks. Another 6 age- and gender-matched subjects with negative treadmill exercise tests were also studied as controls. Compared with control subjects, patients with syndrome X had significantly reduced coronary flow reserve, reduced plasma levels of nitrate and nitrite (NOx), and a reduced plasma L-arginine to asymmetric dimethylarginine (ADMA) ratio (an index of systemic NO metabolism), as well as reduced endothelial function. These patients also had increased plasma levels of ADMA, which is an endogenous inhibitor of NO synthase and of von Willebrand factor, a marker of endothelial injury. Baseline characteristics including exercise performance and coronary flow reserve were similar between enalapril and placebo groups. After an 8-week treatment period, exercise duration (p = 0.001) and coronary flow reserve (p = 0.001) significantly improved with enalapril but not with placebo. Enalapril treatment, but not placebo, reduced plasma von Willebrand factor (p = 0.03) and ADMA levels (p = 0.01) and increased NOx levels (p = 0.01) and the ratio of L-arginine to ADMA (p <0.01). In patients with syndrome X, the plasma NOx level was positively and ADMA level inversely correlated with coronary flow reserve before and after the treatment. In conclusion, long-term ACE inhibitor treatment with enalapril improved coronary microvascular function as well as myocardial ischemia in patients with syndrome X. This may be related to the improvement of endothelial NO bioavailability with the reduction of plasma ADMA levels.

Patients with angiographically proven stent restenoses do not necessarily develop adverse cardiac events. Which clinical, procedural, or angiographic parameters relate to the development of adverse cardiac events among these patients has not been determined. This study included 155 patients (167 stented lesions) with angiographically proven restenosis (≥ 50% diameter stenosis) within the stent or at its margins in routine follow‐up angiograms that was obtained at 6.5 ± 3.6 months after successful stenting. Thirty‐six patients (22%) had adverse cardiac events (including unstable angina necessitating target lesion revascularization, acute myocardial infarction, or cardiac death) during follow‐up and 119 patients (78%) were event‐free. These two groups of patients were compared to determine the parameters related to adverse cardiac events. Univariate determinants of adverse events included hypertension (P = 0.023), unstable angina at initial presentation (P = 0.002), target lesion in proximal left anterior descending artery (P = 0.041), TIMI grade 0–2 flow in follow‐up angiograms (p < 0.001), impaired left ventricular function at follow‐up (P = 0.002), follow‐up minimal lumen diameter ≤ 0.6 mm (P = 0.003), follow‐up diameter stenosis > 75% (P = 0.005), late loss > 2 mm (P = 0.01), and loss index > 1.127 (P < 0.001). Multivariate analysis demonstrated hypertension (odds ratio, OR, = 3.6; P = 0.019), unstable angina at initial presentation (OR = 2.6; P = 0.007), TIMI grade 0–2 flow at follow‐up (OR = 2.8; P = 0.05), impaired LV function at follow‐up (OR = 4.2; P = 0.004), and loss index > 1.127 (OR = 3.6; P = 0.017) as independent risk factors for adverse cardiac events. Classification and regression tree analysis identified loss index > 1.127 and impaired LV function as the two strongest determinant of adverse cardiac event. Therefore, hypertensive patients whose initial clinical presentation were unstable angina should be managed carefully to optimize the angiographic results and, most importantly, followed up more closely for development of impaired LV function after coronary stenting in order to prevent the occurrence of adverse cardiac event at follow‐up. Cathet Cardiovasc Intervent 2002;55:331–337. © 2002 Wiley‐Liss, Inc.

A recent study has demonstrated that the pulsatility of the ascending aorta is a strong predictive factor for restenosis after coronary angioplasty. However, whether the pulsatility of the ascending aorta is still a significant predictor for restenosis in elderly patients with a stiffer aorta is unknown. We investigated the relation between arterial pulsatility in the ascending aorta and restenosis after coronary angioplasty in patients aged >60 years. Eighty-seven consecutive patients (80 men, aged 72.5 ± 5.1 years) with stable angina were included. Before angioplasty, the arterial systolic, diastolic, and mean pressure waveforms of the ascending aorta were measured. We used fractional pulse pressure (PPf, the ratio of pulse pressure to mean pressure) and pulsatility index (PI, the ratio of pulse pressure to diastolic pressure) to estimate the pulsatility of the ascending aorta. Angiographic restenosis occurred in 39 patients. Pulse pressure, PPf, and PI were significantly higher in patients with restenosis after coronary angioplasty (restenosis vs without restenosis: pulse pressure, 77.6 ± 12.2 vs 66.1 ± 15.4 mm Hg [p <0.001]; PPf, 0.80 ± 0.09 vs 0.69 ± 0.11 [p <0.001]; PI, 1.19 ± 0.20 vs 0.98 ± 0.21 [p <0.001]). After multivariate stepwise adjustment of risk factors of restenosis and using receiver-operating characteristic analysis, the odds ratio (OR) of restenosis was: pulse pressure >66 mm Hg, OR 5.88 (95% confidence interval [CI] 2.17 to 15.93); PPf >0.72, OR 13.71 (95% CI 4.81 to 39.05); PI >1.06, OR 13.56 (95% CI 4.67 to 39.38). Moreover, among patients aged >70 years (n = 60), the predictive values of PPf and PI were even higher than those in patients aged ≤70 years (n = 27). Thus, in elderly patients with stable angina, the pulsatility of the ascending aorta is a powerful predictor of restenosis after coronary angioplasty.

The relationship between coronary hemodynamics and left ventricular contractility was studied in 20 patients with syndrome X. Among them, 10 patients with a resting left ventricular ejection fraction (LVEF, by radionuclide method) equal to or greater than the mean value of the whole group (58%) were defined as having relative increased left ventricular contractility (group H), and another 10 patients with relatively normal contractility (50%≤LVEF<58%) were in group N. Eight subjects with normal contractility, exercise test and coronary angiograms served as the control (group C). Baseline great cardiac venous flow (GCVF) was higher in group N than in group H (P<0.05) and C (P<0.05), but similar between group H and C. After dipyridamole infusion (0.56 mg/kg, i.v., for 4 min), maximum GCVF was less in group H than in group N (P<0.001) and C (P<0.001), but similar between group N and C. As compared to group C (3.09±0.35), coronary flow reserve was reduced in both group H (2.34±0.55, P=0.004) and N (2.40±0.36, P=0.001). In all syndrome X patients, resting LVEF was negatively correlated to baseline GCVF (P=0.026) and tended to be positively correlated to baseline coronary vascular resistance (P=0.057). Thus, coronary hemodynamics was altered with left ventricular contractility in syndrome X patients. In these patients, coronary flow reserve was similarly reduced with different underlying mechanisms. The limited increase of GCVF after dipyridamole infusion suggests impaired coronary microvascular dilation capacity in patients with relatively increased left ventricular contractility and the increase of baseline GCVF in those with normal contractility is more likely due to an altered basal myocardial metabolism.

The purpose of the present study was to determine whether coronary microvascular function is impaired in patients with symptomatic mitral valve prolapse (MVP) and whether ischemia-like ECG, if present, is related to coronary microvascular dysfunction. Twenty chest pain patients with normal coronary angiograms and MVP proven by echocardiogram were included. Both treadmill exercise test (TET) and coronary hemodynamic study were done in each patient. Coronary flow reserve (CFR) was determined by measuring coronary sinus flow (CSF) or great cardiac venous flow (GCVF) both at baseline and after dipyridamole 0.56 mg/kg IV for 4 minutes (maximum). All patients were divided into 2 groups with either negative (TET-) or positive results of TET (TET+). Another 10 subjects with atypical chest pain, normal coronary angiograms, echocardiogram and TET were used as controls. There were no differences in GCVF, either at baseline or after dipyridamole infusion, among the 3 groups. Calculated CFR using GCVF was similar among the 3 groups. However, baseline CSF was higher in the TET+ group (TET- vs TET+ vs control: 77 +/- 24 vs 96 +/- 31 vs 75 +/- 12 ml/min, p < 0.05) and maximum CSF was lower in the TET- group (TET- vs TET+ vs control: 167 +/- 25 vs 219 +/- 85 vs 238 +/- 80 ml/min, p < 0.05). Calculated CFR using CSF was significantly reduced in both the TET- (2.26 +/- 0.4) and TET+ groups (2.31 +/- 0.7) as compared with the control subjects (3.18 +/- 0.95, p < 0.01). There were no differences in any of the hemodynamic parameters between the TET- and TET+ groups. Coronary microvascular function could be impaired in patients with symptomatic MVP. Such impairment, when presented, was probably regional and outside the territory of the left anterior descending coronary artery. However, it was irrelevant to the presence of ischemic-like ECG during exercise.

Little information is available concerning the effect of late coronary stenting in patients with recent myocardial infarction, especially long-term results. We retrospectively reviewed our results of 57 stent placements in 52 consecutive patients who received stents at an infarct-related lesion 24 hr to 30 days after an acute myocardial infarctions (median, 14 days). The average age was 67 years; 90% were male. Two patients who suffered from acute stent thrombosis received revascularization again and two early deaths were due to refractory cardiogenic shock before discharge. Mean patient clinical follow-up was 18.3 +/- 6.5 months. There were 1 subacute stent thrombosis, 1 cardiogenic death, and 10 patients (20.8%) in total suffering from angina class II to IV. Angiographic follow-up was performed in 36 patients (80%) at a mean of 7.5 +/- 3.1 months. Of these 36 patients, only 1 (3% of the total population undergoing follow-up angiography) had reocclusion at follow-up, but restenosis existed in 18 patients (50%). We conclude that there is still relatively high incidence of angiographic recurrence that is often silent in long-term follow-up, though the long-term result of late stenting in recent MI is low incidence of reocclusion.

It is not known whether changes in coronary hemodynamics may antedate the development of restenosis after percutaneous coronary transluminal angioplasty (PTCA). The purpose of this study was to evaluate the early change in coronary microvascular function in patients with late restenosis after PTCA.Coronary hemodynamics were studied in series before, immediately after, 2 weeks and 3 months after successful PTCA in 12 male patients with a single lesion of the left anterior descending coronary artery. In each patient, great cardiac venous flow (GCVF) and oxygen content were measured both at baseline and during hyperemia induced by adenosine infusion. The sequential changes of coronary hemodynamics were compared between patients with and without restenosis at 3 months after PTCA,Basic characteristics did not differ between the patients with (n = 6) and those without restenosis (n = 6). Luminal diameter stenosis (in percentage) was also similar between the two groups both before (79.2 +/- 18.4% vs 83.0 +/- 9.6%, p = NS) and up to 2 weeks after PTCA (25.8 +/- 10.9% vs 28.5 +/- 7.9%, p = NS). In patients without restenosis, basal and hyperemic GCVF was unchanged up to 2 weeks after PTCA. There was a significant increase in CFR 3 months after PTCA, In patients with restenosis, basal GCVF was significantly increased and hyperemic GCVF was unchanged immediately after PTCA. However, 2 weeks after PTCA, basal GCVF was decreased while luminal diameter was still preserved. In comparison with those without restenosis, patients with restenosis had significantly lower CFR before (1.98 +/- 0.42 vs 2.69 +/- 0.46, p = 0.019), immediately after (1.47 +/- 0.27 vs 2.24 +/- 0.47, p = 0.006) and 3 months after PTCA (1.51 +/- 0.32 vs 3.40 +/- 0.54, p = 0.001).In patients without restenosis, the recovery of coronary microvascular function was delayed up to 3 months after PTCA. In patients with late restenosis, basal coronary microvascular tone was altered within 2 weeks after PTCA suggesting early deterioration of coronary microvascular function before the development of angiographic restenosis.

To evaluate whether or not coronary microvascular dysfunction is associated with exercise-induced myocardial ischemia in left ventricular dysfunction of unknown cause, both the treadmill exercise test (TET) and coronary hemodynamics were studied in 20 patients with impaired left ventricular ejection fraction (<50% by radionuclide ventriculogram), normal cardiac size, normal coronary angiogram and no evidence of clinical heart failure. Ten subjects with atypical chest pain were studied as the control. Coronary hemodynamics were studied both at baseline and after dipyridamole infusion (0.56mg/kg, i.v. for 4′). There was no difference in age, gender, blood pressure, baseline great cardiac venous flow (GCVF) and coronary vascular resistance between ten patients with a positive TET and the other ten with a negative TET. At baseline, coronary sinus oxygen concentration was increased and myocardial oxygen consumption reduced in patients with a positive TET compared with those with negative a TET. After dipyridamole infusion, maximum GCVF (102±47 vs. 144±31 ml/min, P=0.027) and coronary flow reserve (2.31±0.49 vs. 3.00±0.61, P=0.012) were significantly reduced and minimum coronary vascular resistance was higher (1.00±0.42 vs. 0.63±0.12 mmHg/ml/min, P=0.016) in patients with a positive TET than in those with a negative TET. At follow-up, 40% of patients with a positive TET and 10% of those with a negative TET developed clinical heart failure with a dilated left ventricle during a period of 45 months. Thus, coronary microvascular function is heterogeneous in patients with left ventricular dysfunction of unknown cause. In some of them, coronary microvascular dysfunction could be related to the presence of exercise-induced myocardial ischemia, suggesting that similar pathophysiology underlies the early stage of dilated cardiomyopathy and syndrome X.

This study was to evaluate the dynamic changes in cardiac autonomic control preceding electrocardiographic (ECG) myocardial ischemia in patients with syndrome X. Twenty-four-hour ambulatory ECG was obtained in 34 consecutive patients in a drug-free state. Fourteen (41%) of them, aged 58.8±13.5 years, presented a total of 19 ischemic episodes, mean duration 12.4±19.8 min (ranged 1 to 90 min). Heart rate variability was measured for 24 h; for 3 min and 30 min before, and during the 15 min (in five 3-min intervals) immediately antedating ST segment depression; and for another 3 min after ST segment back to normal. There were significant progressive shortenings in sinus cycle lengths over the 30 min preceding myocardial ischemia (−30 vs −3 minute, 822±32 ms vs 637±23 ins, P<0.05; a decrement of 22.5%). The sinus cycle lengths lengthened after ischemia ceased. High frequency activity, pNNSO and rMSS.D. were significantly reduced from the −30 min baseline to a nidus in the last 3 min before ischemia (P<0.05), whereas low frequency band and low/high frequency ratio did not present significant change. These findings strongly argue that cardiac autonomic control, especially vagal withdrawal, is involved in the pathogenesis of dynamic myocardial ischemia in syndrome X.

Even though the underlying mechanisms of myocardial ischemia may be different, it is difficult to differentiate syndrome X from coronary artery disease (CAD) by means of the treadmill exercise test in elderly patients with chest pain and exercise-induced myocardial ischemia. One hundred sex- and age-matched patients-42 with syndrome X and 58 with CAD-were studied. Another 10 subjects with atypical chest pain, negative treadmill exercise test, and normal-appearing coronary angiograms served as controls. We evaluated the difference in exercise performance between patients with syndrome X and CAD, and the treadmill exercise test was undertaken with modified Bruce protocol within 2 weeks before coronary angiography. Parameters including time to 1 mm ST segment depression (STD), exercise duration (ED), heart rate (HR), systolic blood pressure, rate-pressure product (RPP), and percentage of age-predicted maximum HR (% HR) at different stages of the test were measured and then compared among the three groups of patients. Compared with CAD patients, syndrome X patients had significantly higher HR, % HR, and RPP at the time of 1 mm STD and at peak exercise. The time to 1 mm STD and ED were longer in syndrome X than in CAD patients. However, ED was shorter and HR, % HR, and RPP at peak exercise were similar in syndrome X patients as compared with control subjects. The new criterion of combined ED (> or =315 seconds) and RPP at peak exercise (> or =24,000 beats x mmHg/min) was found to be highly specific (86%) and moderately sensitive (64%) in differentiating syndrome X from CAD patients. The positive likelihood ratio for this criterion was 4.57 and negative likelihood ratio was 0.42. In conclusion, syndrome X patients had better exercise performance than CAD patients, but less ED and similar workload when compared with control subjects. The new criterion proposed in this study may provide a quick and simple way to differentiate syndrome X from CAD in a group of aged and predominantly male patients with chest pain and positive treadmill exercise test.

OBJECTIVE The goals of this study were to compare glucose tolerance in dipper and nondipper hypertensive patients and to explore the cause of glucose intolerance in essential hypertension. RESEARCH DESIGN AND METHODS A total of 50 patients <45 years old who had essential hypertension were recruited and studied by 24-h blood pressure monitoring and an oral glucose tolerance test (OGTT). Autonomic function was assessed with spectral analysis of heart rate variability. RESULTS Dipper hypertensive patients (n = 25) had lower nocturnal blood pressure than nondipper (n = 25) patients. During OGTT, postprandial glucose levels were higher in the nondippers at 0,90, and 120 min (all P < 0.05). Nondippers had a higher fasting insulin/glucose ratio than was apparent in normal control subjects. Despite higher postprandial glucose levels, nondippers had lower postprandial insulin levels. These results suggest that nondippers were insulin resistant and that their pancreatic β-cell function was impaired. For all patients, nocturnal reduction of blood pressure was inversely related to total glucose levels under the OGTT curve and was positively related to postprandial insulin levels. Daytime heart rate did not differ between the dippers and nondippers, but nocturnal heart rate was higher in the nondippers, suggesting that nocturnal sympathetic activities were higher among the nondippers. Spectral analysis of heart rate variability suggests that the nondippers had lower parasympathetic activities and unbalanced sympathetic/parasympathetic outflow. CONCLUSIONS These findings indicate that nondipper hypertensive patients are more glucose intolerant than are dipper patients. The abnormalities of glucose metabolism in nondippers could be explained by insulin resistance and β-cell dysfunction. The results of spectral analysis suggest that abnormal autonomic outflow may represent a possible link between hypertension and associated metabolic dysfunction.

The underlying mechanisms of myocardial ischemia in microvascular angina may include endothelial dysfunction, abnormal smooth muscle tone, and abnormal autonomic control of coronary microvasculatures. This randomized, double-blind, placebo-controlled, crossover study was conducted to evaluate the effect of nicorandil (a nitrate-potassium channel opener) therapy on exercise-induced myocardial ischemia and cardiac autonomic activity in 13 patients with microvascular angina. After a 2-week placebo run-in period, patients were randomly assigned to the first 2-week treatment with nicorandil 5 mg tid or placebo, then crossed over to the second 2-week treatment after a 2-week washout period. Treadmill exercise tests and 24-hour ambulatory electrocardiogram monitoring were performed at the end of each treatment phase. The results showed that both time to 1-mm ST depression and total exercise duration were significantly prolonged with nicorandil treatment compared with placebo (p = 0.026 and 0.036, respectively). Maximum exercise ST depression also tended to be less with nicorandil treatment than with placebo (p = 0.083). Compared with 10 healthy control subjects, study patients had significantly reduced heart rate variability in both low- and high-frequency bands while receiving placebo. Nicorandil treatment did not change the altered heart rate variability in either time domain or spectral analysis. Systemic hemodynamics were also unchanged with nicorandil treatment. Thus, 2-week oral nicorandil therapy moderately improved exercise-induced myocardial ischemia without modifying the already altered cardiac autonomic activity, suggesting that nicorandil might have a direct vasodilatory effect on coronary microvasculatures in patients with microvascular angina.

Two patients with new coronary stenotic lesions subsequently developed proximal to the sites accepting directional coronary atherectomy (DCA) are reported. One lesion developed at the left main coronary artery and the other at the proximal segment of the left anterior descending artery. The mechanisms of the development of such new stenotic lesions after DCA were studied and procedure-related mechanical trauma over the proximal segment of the primary lesion may be the possible mechanism for such complication.