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Ethnic differences in the pathobiology of acute coronary syndromes (ACS) have not been systematically studied. We compared the underlying mechanisms of ACS between Asians and Whites. ACS patients with the culprit lesion imaged by optical coherence tomography were included. Patients were stratified into ST-elevation myocardial infarction (STEMI) and non-ST-elevation-ACS (NSTE-ACS), and baseline characteristics, underlying mechanisms of ACS, and culprit plaque characteristics were compared between Asians and Whites. Of 1,225 patients, 1,019 were Asian (567 STEMI and 452 NSTE-ACS) and 206 were White (71 STEMI and 135 NSTE-ACS). Asians had more diabetes and hypertension among STEMI patients; among NSTE-ACS patients, Asians had higher prevalence of diabetes and renal insufficiency, and lower prevalence of hyperlipidemia. There were no differences in the incidence of plaque rupture, plaque erosion and calcified plaque between Asians and Whites with STEMI (61.2%, 28.6%, 10.2% vs 46.5%, 38.0%, 15.5%, respectively, p = 0.055). Among NSTE-ACS patients, there was a significant difference between Asians and Whites (40.5%, 47.6%, 11.9% vs 27.4%, 48.9%, 23.7%, respectively, p = 0.001). After adjustment for clinical confounders, the risk of plaque rupture (p = 0.713), plaque erosion (p = 0.636), and calcified plaque (p = 0.986) was similar between the groups with STEMI. In NSTE-ACS patients, the only difference was an increased risk of calcified plaque in Whites (odds ratio: 2.125, 95% confidence interval: 1.213 to 3.723, p = 0.008). In conclusion, after adjustment for clinical confounders, Asian and White patients presenting with STEMI and NSTE-ACS showed similar underlying mechanisms of ACS, except for a higher risk of calcified plaque in Whites with NSTE-ACS.

"Early repolarization" (ER) is a frequent finding at standard electrocardiogram (ECG). In this study we assessed whether ER is associated with an increased risk of events, as recently suggested by some studies. We prospectively enrolled 4,176 consecutive subjects without any heart disease who underwent routine ECG recording. ER was diagnosed in case of typical concave ST-segment elevation ≥0.1 mV; a J wave was diagnosed when the QRS showed a notch or a slur in its terminal part. In this study we compared the 6-year outcome of all 687 subjects with ER/J wave and 687 matched subjects without ER/J wave (controls). Both groups included 335 males and 352 females, and age was 48.8 ± 18 years. Overall, 145 deaths occurred (11%), only 11 of which attributed to cardiac causes. No sudden death was reported. Cardiac deaths occurred in 5 (0.8%) and 6 (0.9%) ER/J wave subjects and controls, respectively (odds ratio [OR] 0.85, 95% confidence interval [CI] 0.26 to 2.80, p = 0.79). Both ER (OR 1.68, 95% CI 0.21 to 13.3, p = 0.62) and J wave (OR 0.91, 95% CI 0.28 to 3.00, p = 0.88) showed no association with cardiac death. Total mortality was 11.5% in the ER/J wave group and 10.6% in the control group (OR 1.10, 95% CI 0.78 to 1.56, p = 0.58). Both ER (OR 0.44, 95% CI 0.16 to 1.24, p = 0.12) and J wave (OR 1.20, 95% CI 0.85 to 1.70, p = 0.30) showed also no association with all-cause death. In subjects without any evidence of heart disease, we found no significant association of ER/J wave with the risk of cardiac, as well as all-cause, death at medium-term follow-up.

In this study, we aim to assess whether remote ischemic preconditioning (RIPC) reduces platelet activation during coronary angiography (CA) and/or percutaneous coronary interventions. We studied 30 patients who underwent CA because of a suspect of stable angina. Patients were randomized to RIPC (3 short episodes of forearm ischemia) or sham RIPC (controls) before the procedure. Blood samples were collected at baseline, at the end of the procedure, and 24 hours later. Monocyte-platelet aggregate (MPA) formation and platelet CD41 in the MPA gate and CD41 and CD62 expression in the platelet gate were assessed by flow cytometry, in the absence and in the presence of adenosine diphosphate (ADP) stimulation. A significant increase in platelet activation occurred during the invasive procedure in controls, which persisted at 24 hours. However, compared with controls, RIPC group showed no or a lower increase in platelet variables, including MPA formation (p

Our study aimed to elucidate mechanisms underlying discordance between fractional flow reserve (FFR) and hyperemic stenosis resistance (hSR) in some patient subsets. To do this, we enrolled 30 consecutive patients with stable angina or non-ST elevation myocardial infarction (non-STEMI) and with a nonculprit intermediate coronary lesion (40% to 70%) by coronary angiography. We measured aortic pressure, flow velocity, and pressure distal to lesion simultaneously at basal level and during adenosine-induced (fixed intracoronary dose of 120 μg) hyperemia using a dual-sensor-equipped guidewire. Microvascular resistance (MR; pressure distal to lesion/flow velocity, mm Hg/cm/s) and variation (Δ) in MR levels were calculated both at baseline and after hyperemia, whereas FFR (cutoff0.80) and hSR [(aortic pressure - pressure distal to lesion)/flow velocity, cutoff0.80 mm Hg/cm/s] were assessed after intracoronary adenosine. Twenty-three patients (76.7%) showed concordance and 7 patients (23.3%) showed discordance between FFR and hSR (all cases with FFR0.80 and hSR0.80). Discordant patients presented more frequently with non-STEMI (85.7% vs 39.1%, p = 0.04), significantly higher C-reactive protein serum levels (median [interquartile range] 5.9 [5.1 to 6.8] vs 4.9 [3.7 to 6.2] mg/L, p = 0.007), and lower ΔMR (p = 0.03) values compared with concordant patients. In conclusion, patients with non-STEMI and those with increased C-reactive protein levels show a lower reduction in MR after intracoronary adenosine-induced hyperemia, leading to FFR underestimation.

Heart rate variability (HRV) and systemic markers of inflammation have prognostic value in patients with unstable angina pectoris (UAP). However, it is unknown whether any relation exists between HRV parameters and indexes of inflammation in this clinical context. We assessed HRV on 24-hour electrocardiographic Holter recordings, performed within 24 hours of admission, and measured C-reactive protein (CRP) serum levels by a high-sensitivity assay on admission, in 531 patients with UAP (65 +/- 10 years of age; 347 men) who were enrolled in the prospective multicenter study Stratificazione Prognostica dell'Angina Instabile (SPAI). A significant inverse correlation was found between CRP levels and all HRV parameters, with the highest r coefficient shown with SD of all RR intervals (r = -0.23; p < 0.001) in the time domain and with very low-frequency amplitude (r = -0.22; p < 0.001) in the frequency domain. When patients were categorized into 4 groups according to CRP quartile levels, statistically significant lower HRV values were observed in the upper CRP quartile. On separate multiple regression analyses, including the most important clinical and laboratory variables, SD of all RR intervals and very low-frequency amplitude were the most significant predictors of increasing CRP levels (p < 0.001 for the 2 comparisons). In contrast, in models with SD of all RR intervals and very low-frequency amplitude as dependent variables, CRP was a strong predictor of impaired cardiac autonomic function (p < 0.001 for the 2 comparisons). Thus, our data show that, in patients with UAP, high levels of serum CRP levels are significantly associated with decreased HRV, suggesting a possible pathophysiologic link between cardiac autonomic dysfunction and inflammatory activity. (c) 2006 Elsevier Inc. All rights reserved.

Laser atherectomy might decrease procedural complications during percutaneous coronary intervention (PCI) of degenerated saphenous vein grafts (SVGs) in case of unstable or thrombotic lesions because of its ability to debulk and vaporize thrombus. We aimed at prospectively evaluating the safety and efficacy of excimer laser coronary angioplasty (ELCA) as a primary treatment strategy in consecutively unstable patients undergoing PCI of degenerated SVG lesions. Seventy-one consecutive patients with non-ST elevation acute coronary syndrome (mean age 69 ± 10 years, 66 men [89%]) undergoing PCI of degenerated SVG were enrolled in a prospective case-control registry, using 2 different distal protection devices (DPDs; FilterWire EZ [Boston Scientific, Natick, Massachusetts; n = 24] and SpiderRX [Ev3, Plymouth, Minnesota; n = 23]) or ELCA (n = 24). Primary end points of the study were incidence of angiographic microvascular obstruction (Thrombolysis In Myocardial Infarction flow grade of

Patients with microvascular angina (MVA) often have persistence of symptoms despite full classical anti-ischemic therapy. In this study, we assessed the effect of ivabradine and ranolazine in MVA patients. We randomized 46 patients with stable MVA (effort angina, positive exercise stress test [EST], normal coronary angiography, coronary flow reserve2.5), who had symptoms inadequately controlled by standard anti-ischemic therapy, to ivabradine (5 mg twice daily), ranolazine (375 mg twice daily), or placebo for 4 weeks. The Seattle Angina Questionnaire (SAQ), EuroQoL scale, and EST were assessed at baseline and after treatment. Coronary microvascular dilation in response to adenosine and to cold pressor test and peripheral endothelial function (by flow-mediated dilation) were also assessed. Both drugs improved SAQ items and EuroQoL scale compared with placebo (p0.01 for all), with ranolazine showing some more significant effects compared with ivabradine, on some SAQ items and EuroQoL scale (p0.05). Time to 1-mm ST-segment depression and EST duration were improved by ranolazine compared with placebo. No effects on coronary microvascular function and on flow-mediated dilation were observed with drugs or placebo. In conclusion, ranolazine and ivabradine may have a therapeutic role in MVA patients with inadequate control of symptoms in combination with usual anti-ischemic therapy.

Endothelial dysfunction can predict cardiovascular outcomes in several populations of patients. The aim of this study was to assess the severity, time course, and clinical implications of endothelial dysfunction in patients with non-ST-segment elevation (NSTE) acute coronary syndromes (ACS). Sixty patients with NSTE ACS (mean age 62 ± 8 years, 44 men) and 40 controls with stable coronary artery disease (CAD) (mean age 63 ± 10 years, 27 men) were studied. In patients with NSTE ACS and in those with stable CAD, endothelial function was assessed12 hours after admission and at 3-month follow-up by measuring right brachial artery dilation after 5 minutes of forearm ischemia (flow-mediated dilation [FMD]). Clinical outcomes were assessed after a median follow-up period of 32 months (range 14 to 36). The primary end point was a combination of cardiac death or readmission for new ACS or recurrence of angina pectoris. FMD on admission was significantly lower in patients with NSTE ACS compared to those with stable CAD (2.1 ± 1.2% vs 4.8 ± 1.9%, p0.001). FMD improved significantly at 3-month follow-up in patients with NSTE ACS, becoming comparable to that in patients with stable CAD (5.7 ± 2.6% vs 5.5 ± 1.7%, p = 0.93). During follow-up, 14 cardiac events (23%) occurred in patients with NSTE ACS. On multivariate analysis, only diabetes (hazard ratio 18.1, 95% confidence interval 3.9 to 83.9, p0.001) and FMD at 3 months (hazard ratio 0.78, 95% confidence interval 0.61 to 0.99, p = 0.04) were independent predictors of the primary end point in patients with NSTE ACS. In conclusion, endothelial function is markedly impaired in the acute phase of NSTE ACS but improves significantly at 3-month follow-up. In patients with NSTE ACS, FMD at 3 months after the acute event is a significant independent predictor of cardiac outcomes.

The success rate of recanalization of coronary chronic total occlusion (CTO) has improved in recent years, but the clinical benefit associated with successful CTO recanalization in the drug-eluting stent (DES) era is not well known. A cohort of 317 consecutive patients (mean age 65 ± 10, 84% men) with CTOs (defined as Thrombolysis In Myocardial Infarction [TIMI] flow grade 0 and duration >3 months) of native coronary vessels in which percutaneous coronary intervention was attempted was enrolled from June 2005 to March 2009. All successful procedures (196 patients) were performed by DES implantation. The incidence of major adverse cardiac events (MACEs; a composite of cardiac death, myocardial infarction, and repeat revascularization) was assessed during a mean follow-up period of 3 years. MACE predictors were assessed in clinical, angiographic, and procedural data, including procedural success. Patients with successful percutaneous coronary intervention experienced a significantly lower MACE rate compared to those with failed procedures (17 [9%] vs 32 [26%], p = 0.008). Patients with multivessel disease experienced MACEs more frequently than those with single-vessel disease (45 [22%] vs 4 [4%], p = 0.002). On multiple Cox regression analysis, the presence of multivessel disease and CTO opening failure were independent predictors of MACEs (hazard ratio 2.31, 95% confidence interval 1.17 to 4.96, p = 0.01, and hazard ratio 1.81, 95% confidence interval 1.33 to 4.12, p = 0.02, respectively). The worst prognosis was confined to patients with multivessel disease and failed procedures (hazard ratio 2.73, 95% confidence interval 1.21 to 3.92, p = 0.03). In conclusion, successful recanalization of CTOs with DES translates into a reduction of the 3-year MACE rate compared to failed procedures, and the worst prognosis is observed in patients with failed procedures and multivessel disease, a notion that might be taken into account in the management of patients with coronary CTOs.

Patients with cardiac syndrome X (CSX) have an excellent long-term prognosis, but a significant number show worsening angina over time. Previous studies have found a significant impairment of cardiac uptake of iodine-123-meta-iodobenzylguanidine (MIBG) on myocardial scintigraphy, indicating abnormal function of cardiac adrenergic nerve fibers. The aim of this study was to assess whether cardiac MIBG results can predict symptomatic outcome in patients with CSX. Cardiac MIBG scintigraphy was performed in 40 patients with CSX (mean age 58 ± 5 years, 14 men). Cardiac MIBG uptake was measured by the heart/mediastinum uptake ratio and a single photon-emission computed tomographic regional uptake score (higher values reflected lower uptake). Clinical findings, exercise stress test parameters, sestamibi stress myocardial scintigraphy, and C-reactive protein serum levels were also assessed. At an average follow-up of 79 months (range 36 to 144), no patient had died or developed acute myocardial infarction. Cardiac MIBG defect score was significantly lower in patients with worsening versus those without worsening of angina status (13 ± 7 vs 38 ± 28, p = 0.001), in those with versus those without hospital readmission because of recurrent chest pain (15 ± 9 vs 35 ± 29, p = 0.01), and in those who underwent versus those who did not undergo repeat coronary angiography (11 ± 7 vs 36 ± 27, p = 0.001). Significant correlations were found between quality of life (as assessed by the EuroQoL scale) and heart/mediastinum ratio (r = 0.48, p = 0.002) and cardiac MIBG uptake score (r = -0.69, p0.001). No other clinical or laboratory variable showed a significant association with clinical end points. In conclusion, in patients with CSX, abnormal function of cardiac adrenergic nerve fibers, as assessed by an impairment of cardiac MIBG uptake, identifies those with worse symptomatic clinical outcomes.

Myocardial no-reflow may negate the benefit of urgent coronary revascularization in patients with acute ST-elevation myocardial infarction (STEMI). Among its pathogenetic mechanisms, distal embolization is of prominent importance and several studies have shown that a high coronary thrombotic burden is associated with distal embolization. We aimed at assessing predictors of angiographic thrombus grade in patients undergoing primary percutaneous coronary intervention. Ninety-one patients (62 +/- 12 years old, 79% men) presenting for a first STEMI and undergoing urgent coronary angiography within 12 hours from onset of symptoms were consecutively included in the study. Thrombus grade was evaluated by angiography according to the Gibson score and patients were allocated to the high thrombus grade (HTG; score 4 to 5) group or to the low thrombus grade (score 0 to 3) group. Variables predicting angiographic thrombus grade were assessed among clinical, angiographic, procedural, and laboratory data. Sixty-four patients (61 +/- 12 years old, 78% men) presented with HTG, whereas 27 patients (63 +/- 10 years old, 80% men) presented with low thrombus grade. Patients an HTG showed a significantly higher white blood cell count (12.5 +/- 4.8 vs 10.5 +/- 2.9, p = 0.015). Aspirin and beta-blocker therapy before admission were less frequently taken in the HTG group (5% vs 26% and 7% vs 23%, respectively, p = 0.01 and p = 0.03). At multivariate analysis, lack of previous therapy with aspirin was the only independent predictor of an HTG (odds ratio 6.14, 95% confidence interval 1.09 to 34.67, p = 0.04). In conclusion, previous aspirin therapy is associated with a decrease in angiographic thrombus grade in patients with STEMI treated with primary percutaneous coronary intervention, thus further priming efforts for appropriate use of aspirin in primary prevention of a first STEMI.

Heart failure is a complex syndrome characterized by impaired emptying and/or impaired filling of the heart chambers. The use of parameters of diastolic function has provided novel tools for risk stratification and management of patients with heart failure. This study evaluated the potential correlation between apoptosis at time of death and left ventricular (LV) diastolic function after acute myocardial infarction. We selected, at routine postmortem examination, 14 subjects who died 10 to 62 days after an acute myocardial infarction and had an available echocardiographic report from the most recent hospital admission. The apoptotic rate was calculated at the region bordering the infarct, using co-localization of in situ end-labeling for deoxyribonucleic acid fragmentation and immunohistochemistry for caspase-3. Transthoracic echocardiographic studies were retrospectively reevaluated and pulse-wave Doppler spectra of mitral inflow were analyzed. LV diastolic function was assessed by measuring the ratio of E peak velocity to A peak velocity and E-wave deceleration time; a ratio of E peak velocity to A peak velocity ≥2 and deceleration time

Experimental studies suggest that alcohol may have protective effects similar to that of ischemic preconditioning (IPC). The acute effects of alcohol on IPC in humans, however, are poorly known. In this study, we assessed the effect of alcohol administration on the warm-up phenomenon, as an expression of IPC, in patients with stable coronary artery disease (CAD). We randomized 45 stable CAD patients with positive (ST-segment depressionor =1 mm) exercise stress test to 1 of 3 groups of 15 patients each: (1) group 1 = 60 cc of gin (18.5 g of ethanol); (2) group 2 = 180 cc of red wine (18.9 g of ethanol); and (3) group 3 = placebo (120 cc of water). A first exercise test was performed 15 minutes after beverage administration. In those with a positive exercise test (13, 14, and 14 patients in the gin, wine, and placebo groups, respectively), a second exercise test was performed 15 minutes after the end of the first one. On the first test, there were no differences among groups in rate pressure product and time of exercise at 1-mm ST-segment depression, as well as in maximal ST segment depression. Furthermore, an improvement of the ischemic exercise variables was observed in each group, without any statistically significant differences among them. In conclusion, our data show that, in stable CAD patients, the acute intake of low doses of alcohol does not significantly influence IPC, as expressed by the warm-up phenomenon on exercise stress testing.

To evalutate whether Holter electrocardiographic monitoring may improve the detection of ST-segment depression in patients with anginal chest pain and normal coronary arteries, we performed symptom-limited exercise testing and 24-hour Holter monitoring in a group of 38 such patients (27 women, age 54 +/- 8 years). Patients were divided into 2 groups: group X1 included 28 patients with and group X2 10 patients without significant ST-segment depression during exercise testing. There were no significant differences between the 2 groups in age, gender, characteristics of chest pain, exercise duration, heart rate (HR), and blood pressure at peak exercise, but anginal pain during exercise testing was reported by 10 patients of group X1 (36%) and 9 of group X2 (90%) (p < 0.01). Episodes of ST-segment depression on Holter monitoring were found in 17 patients of group X1 (61%) and in 5 patients of group X2 (50%) (p = NS). There were no differences between the 2 groups in daily number of ST episodes (3.6 +/- 4 vs 2.8 +/- 5 episodes per patient), symptomatic episodes (8% vs 18%), and duration of the episodes. On average, HR increased significantly, in a similar way, from 15 minutes before ST-segment depression to 1-mm ST in both groups, and its value at the onset of ischemia was similar in the 2 groups (102 +/- 22 vs 109 +/- 18 beats/min, p = NS). Finally, HR at 1-mm ST during Holter monitoring was significantly lower than that observed at 1-mm ST during exercise testing (127 +/- 16 beats/min, p less than or equal to 0.01) in group X1, and it was also lower than that observed at peak exercise (136 +/- 22 beats/min, p less than or equal to 0.01) in group X2. In conclusion, Holter monitoring can significantly Increase the detection of ST-segment depression in patients with anginal pain and normal coronary arteries, indicating a cardiac, although not necessarily ischemic, origin of the pain. Indeed, 50% of our patients with negative symptom-limited exercise testing showed spontaneous ST changes, compatible with transient myocardial ischemia, during daily activities. Differences in the response of coronary microvascular tone to exercise testing and to stimuli operating during daily life are likely to play a significant role in determining these findings. (C) 1997 by Excerpta Medica, Inc.

Location, severity, duration, and time course of pain were assessed in 104 consecutive patients with either first or second, anterior or inferior Q-wave acute myocardial infarction (AMI). Pain severity was assessed using a visual analog scale. Pain location and radiation were similar in 48 patients with anterior and 56 patients with inferior wall AMI. Pain duration (6.1 +/- 6.4 vs 6.5 +/- 5.4 hours, p = NS) and severity (68 +/- 21 vs 61 +/- 21 mm, p = NS) were also similar. The pain was continuous in 34 patients with anterior (71%) and in 42 with inferior (75%) wall AMI. Among the 41 patients who did not receive thrombolytic therapy, 18 patients with continuous pain had a higher creatine kinase peak level than the remaining 23 patients with intermittent pain or preinfarction angina, or both (2,065 +/- 1,017 vs 1,162 +/- 994 IU, p 1 AMI, different locations of the infarction pain were highly predictive of ischemia occurring in different myocardial regions. Finally, patients with preinfarction angina or intermittent pain tended to have smaller infarcts.

The term "heart rate turbulence" (HRT) indicates the physiologic changes in the sinus cycle that follow a ventricular premature complex; impaired HRT denotes abnormalities in cardiac autonomic function. To investigate whether HRT is impaired in patients with stable coronary artery disease (CAD), we studied 29 patients with documented CAD and frequent (/=30/hour) ventricular premature complexes on Holter monitoring and 31 patients with frequent ventricular arrhythmias but normal hearts (NH-VA). HRT and heart rate variability analyses were analyzed on 24-hour Holter recordings. HRT variables differed significantly between the 2 groups (turbulence onset -0.20 +/- 1.7% vs -0.67 +/- 2.2%, p = 0.00001; turbulence slope 2.83 +/- 1.9 vs 10.83 +/- 7.4 ms/RR, p = 0.0001 in patients with CAD and NH-VA, respectively). The difference was independent of a history of previous myocardial infarction, left ventricular function, and age. Top quartile turbulence onset values (-0.26%) and bottom quartile turbulence slope values (2.12 ms/RR) had similar predictive power in discriminating between patients with CAD and NH-VA (positive predictive value 86.7%, negative predictive value 64.4% for both). Among heart rate variables, bottom quartile SD of all RR intervals values (96.3 ms) only had the same power of HRT variables in discriminating between patients with CAD and NH-VA. Thus, our data show that HRT variables are impaired in patients with CAD patients versus those with NH-VA, indicating abnormalities in the control of short-term cardiac autonomic mechanisms resulting in decreased vagal activity with likely predominant sympathetic activity.

This study was aimed at establishing the relation between baseline C-reactive protein levels and 12-month outcome in patients with unstable angina successfully treated with coronary artery stent implantation. Our results suggest that in patients with unstable angina and 1-vessel coronary disease successfully treated with coronary artery stent implantation, normal baseline serum levels of C-reactive protein identify a subgroup of patients at low risk of cardiac events during follow-up.

Plasma levels of C-reactive protein were measured 72 hours after successful coronary artery stenting in 76 patients with stable angina pectoris. At 12-month follow-up, the cumulative event rate was higher in patients with abnormal levels of C-reactive protein than that observed in patients with normal C-reactive protein who were event free.

An increased sensitivity to painful stimuli and an abnormal cardiac autonomic function have previously been reported in patients with angina and angiographically normal coronary arteries, a syndrome that mainly affects postmenopausal women. In this study we compared both general sensitivity to pain, by evaluating time to forearm ischemic pain (FIP) provoked by sphygmomanometer cuff inflation, and cardiac autonomic function, by measuring heart rate variability (HRV), and QT and QT(c) intervals on 24-hour Holter recordings, in 25 postmenopausal women with angina and normal coronary arteries and in 22 healthy postmenopausal women. Compared with controls, patients had a reproducible strikingly lower time to FIP (149 +/- 121 vs 295 +/- 158 seconds, p

Emerging evidence suggests that neointimal degenerative changes with development of neoatherosclerosis (NA) may represent an important mechanism for late stent failure. The aim of the present study was to investigate the relation between degree of neointimal hyperplasia and incidence and characteristics of NA using optical coherence tomography. We identified a total of 252 stents with mean neointimal thickness (NIT)100 μm in 212 patients: 100 bare metal stents (BMSs) and 152 drug-eluting stents (DESs). Based on the values of mean NIT, we divided stents into tertiles and compared neointimal characteristics among the 3 groups. NA was defined as the presence of lipid-laden intima and/or calcification inside the stent. In both BMS and DES, there was a difference in the prevalence of lipid-laden intima among the tertiles (18.2% vs 36.4% vs 47.1%, p = 0.042 [BMS]; 19.6% vs 56.9% vs 88.0%, p0.001 [DES]). However, no difference in the prevalence of in-stent calcification was observed (21.2% vs 21.2% vs 2.9%, p = 0.053 [BMS]; 5.9% vs 9.8% vs 2.0%, p = 0.252 [DES]). In a multivariate model adjusting for stent type, follow-up duration, conventional coronary risk factors, statin, and angiotensin-converting enzyme inhibitor or angiotensin II receptor blockade use, mean NIT was independently associated with the presence of NA (odds ratio 2.53, 95% confidence interval 1.96 to 3.27, p0.001). This study demonstrates the presence of a positive correlation between degree of neointimal hyperplasia after stent implantation and presence of lipid-laden intima. This association is independent from stent type and time from implantation and suggests a possible pathogenic link between the two processes.

This study assesses regional coronary flow reserve using adenosine thallium-201 scintigraphy early and 6 months after angiographically successful percutaneous transluminal coronary angioplasty (PTCA) or stent implantation. Seventeen consecutive men with a significant isolated left anterior descending coronary artery stenosis were scheduled for repeat coronary angiography and adenosine-planar thallium-201 scintigraphy within 24 hours and 6 months after successful PTCA (n = 8) or stent implantation (n = 9). After background subtraction, left ventricular segmental uptake was semiquantitatively assessed on thallium images. The perfusion defect severity was scored from 0 (normal) to 3. Coronary angiograms were analyzed using an automated edge contour detection computer analysis system. Data are expressed as mean value +/- 1 SD, and proportions as percentage. The residual narrowing was 17 +/- 8% after PTCA and 9 +/- 2% after stent implantation (p = 0.02). Twenty-four hours after the procedure, hypoperfused segments were detected in all patients (100%) and in 4 patients (44%) (p = 0.05), respectively. The total number of hypoperfused segments was greater after PTCA than after stent implantation (16 [40%] vs 7 [16%], p = 0.001, respectively) as was the perfusion defect severity (4.4 +/- 3.1 vs 1 +/- 1.2, p = 0.006). Six months after the procedure, 3 of the 5 patients who had undergone PTCA without restenosis still had reversible perfusion defects. None of the stent-treated patients had restenosis or reversible perfusion defects (p = 0.05). Among PTCA-treated patients without restenosis, the total number of hypoperfused segments and the perfusion defect severity were 9 of 25 (36%) and 0.8 +/- 0.8, respectively. Thus, a regional reduction in coronary flow reserve, occasionally observed early after successful stent implantation, is probably due to a transient alteration of small coronary vessels, as was also supported by the absence of perfusion defects 6 months after the procedure. The more severe impairment of regional coronary flow reserve observed early after successful PTCA is probably also due to angiographic underestimation of the residual stenosis, as suggested also by the persistence of reversible perfusion defects 6 months after the procedure in a few patients.