Lifestyle Modification in the Management of Metabolic Syndrome: Statement From Korean Society of CardioMetabolic Syndrome (KSCMS).

With the recent rapid increase in obesity worldwide, metabolic syndrome (MetS) has gained significant importance. MetS is a cluster of obesity-related cardiovascular risk factors including abdominal obesity, atherogenic dyslipidemia, high blood pressure and impaired glucose tolerance. MetS is highly prevalent and strongly associated with an increased risk of developing diabetes and cardiovascular disease, putting a great burden on human society. Therefore, it is very important to reduce MetS risk, which can improve patients' cardiovascular prognosis. The primary and most effective strategy to control each component of MetS is lifestyle change such as losing body weight, keeping regular exercise, adopting a healthy diet, quitting smoking and alcohol drinking in moderation. Many studies have shown that lifestyle modification has improved all components of MetS, and reduces the incidence of diabetes and cardiovascular disease. Here, the Korean Society of CardioMetabolic Syndrome has summarized specific and practical methods of lifestyle modification in the management of MetS in the healthcare field.

Irreversible effects of long-term chronic smoking on arterial stiffness: An analysis focusing on ex-smokers among otherwise healthy middle-aged men.

Objective: Smoking is a modifiable cardiovascular risk factor closely related to arterial stiffness (AS). However, data are lacking regarding the chronic effects of smoking on AS, especially in ex-smoker (ES) who faces remnant cardiovascular risk when compared to never-smokers (NS).Methods: Among 1722 health screening participants, we retrospectively evaluated 652 healthy men with different smoking history [240 current smoker (CS) vs. 228 ES vs. 184 NS]. To assess AS, augmentation index (AIx), pulse pressure amplification (PPamp), and carotid-femoral pulse wave velocity (cfPWV) were measured and compared.Results: Baseline characteristics were similar except age and triglyceride level. AIx was lowest in NS, followed by ES, and was highest in CS. PPamp was highest in NS, lowest in CS, and ES was of intermediate level. The differences were more robust after adjustment for baseline covariates (AIx, p = 0.005; PPamp: p = 0.001). On the other hand, no significant intergroup difference was observed for cfPWV in our middle-aged population. With the regression analyses revealing an independent association between smoking duration and AS in ES, subgroup analysis demonstrated that long-term ES (smoking duration ≥20 years) had significantly higher AS than short-term ES (<20 years) and NS, approaching levels comparable to CS (AIx and PPamp: p < 0.0001).Conclusions: Our study demonstrated impaired arterial elastic properties in long-term ES, suggesting that AS caused by chronic smoking might be irreversible even after smoking cessation. Further longitudinal studies are warranted to determine the impacts of past smoking on AS and its clinical relevance.

A Case Report of Primary Pericardial Malignant Mesothelioma Treated with Pemetrexed and Cisplatin.

Primary pericardial malignant mesothelioma (PPM) is a very rare malignancy, with an incidence of less than 0.002% and represents less than 5% of all mesotheliomas. The cause of pericardial mesothelioma is uncertain that differ from pleural mesothelioma which is associated with asbestos exposure. This malignancy is terribly aggressive and has very poor prognosis with less than six months of overall survival. We present a case of a 71-year-old woman who was diagnosed with cardiac tamponade caused by PPM and received chemotherapy with pemetrexed and cisplatin for six months. During two years she was alive without disease progression. To better understand the clinical, pathologic features and treatment outcome of this entity, we reviewed 23 cases described in the English literature from 2009, together with our case, provided a total of 24 cases. Based on this review, we suggest that PPM must be considered in patients who have unexplained massive pericardial effusion and recommend chemotherapy with pemetrexed and cisplatin for the better outcome of PPM.

Distal coronary embolization following acute myocardial infarction increases early infarct size and late left ventricular wall thinning in a porcine model.

BACKGROUND: Distal coronary embolization (DCE) of thrombotic material occurs frequently during percutaneous interventions for acute myocardial infarction and can alter coronary flow grades. The significance of DCE on infarct size and myocardial function remains unsettled. The aims of this study were to evaluate the effects of DCE sufficient to cause no-reflow on infarct size, cardiac function and ventricular remodeling in a porcine acute myocardial infarction model. METHODS AND RESULTS: Female Yorkshire pigs underwent 60 min balloon occlusion of the left anterior descending coronary artery followed by reperfusion and injection of either microthrombi (prepared from autologous porcine blood) sufficient to cause no-reflow (DCE), or saline (control). Animals were sacrificed at 3 h (n = 5), 3 days (n = 20) or 6 weeks (n = 20) post-AMI. Cardiovascular magnetic resonance (CMR), serum troponin-I, and cardiac gelatinase (MMP) and survival kinase (Akt) activities were assessed. At 3d, DCE increased infarct size (CMR: 18.8% vs. 14.5%, p = 0.04; serum troponin-I: 13.3 vs. 6.9 ng/uL, p < 0.05) and MMP-2 activity levels (0.81 vs. 0.49, p = 0.002), with reduced activation of Akt (0.06 versus 0.26, p = 0.02). At 6 weeks, there were no differences in infarct size, ventricular volume or ejection fraction between the two groups, although infarct transmurality (70% vs. 57%, p< 0.04) and ventricular thinning (percent change in mid anteroseptal wall thickness:-25.6% vs. 0.7%, p = 0.03) were significantly increased in the DCE group. CONCLUSIONS: DCE increased early infarct size, but without affecting later infarct size, cardiac function or ventricular volumes. The significance of the later remodelling changes (ventricular thinning and transmurality) following DCE, possibly due to changes in MMP-2 activity and Akt activation, merits further study.

Perlecan heparan sulfate proteoglycan is a critical determinant of angiogenesis in response to mouse hind-limb ischemia.

BACKGROUND: Perlecan is a heparan sulfate proteoglycan (HSPG) constituent of the extracellular matrix with roles in cell growth, differentiation, and angiogenesis. The role of the HS side chains in regulating in vivo angiogenesis after hind-limb ischemia is unknown. METHODS: Heparan sulfate (HS)-deficient perlecan (Hspg2(Δ3/Δ3)) mice (n = 35), containing normal perlecan core protein but deficient in HS side chains, and wild-type (n = 33) littermates underwent surgical induction of hind-limb ischemia. Laser Doppler perfusion imaging (LDPI) and contrast-enhanced ultrasonography (CEU) provided serial assessment of hind-limb perfusion. Harvested muscles underwent immunostaining for endothelial cell density (CD31), real-time reverse transcription polymerase chain reaction RT-PCR for vascular endothelial growth factor (VEGF) mRNA expression and western blot analysis for VEGF and fibroblast growth factor (FGF)2 protein expression at days 2 and 28. RESULTS: Serial LDPI showed significantly greater perfusion recovery in ischemic limbs of wild-type compared with Hspg2(Δ3/Δ3) mice. CEU showed that normalized microvascular perfusion was increased in wild-type compared with Hspg2(Δ3/Δ3) mice at day 28 (0.67 ± 0.12 vs 0.26 ± 0.08; P = 0.001). CD31-positive cell counts were significantly higher in wild-type compared with Hspg2(Δ3/Δ3) mice on day 28 (122 ± 30 cells vs 84 ± 34 cells per high-power field [HPF]; P < 0.05). Endogenous VEGF mRNA expression (P < 0.05) and VEGF protein expression (P < 0.002) were significantly decreased in the ischemic limbs of Hspg2(Δ3/Δ3) mice compared with wild-type mice at day 2 and day 28, respectively. FGF2 protein expression showed no significant differences. CONCLUSIONS: These results suggest that the HS side chains in perlecan are important mediators of the angiogenic response to ischemia through a mechanism that involves upregulation of VEGF expression.

Unexpected calcification after direct intravascular injection of autologous bone marrow-derived cells in a chronic total occlusion model.

AIMS: Patients with symptomatic chronic total occlusions (CTO) remain a therapeutic challenge. Enhancement of intraluminal neovascularisation by pro-angiogenic therapies has been proposed as a new strategy to improve percutaneous revascularisation. The aim of this study was to investigate the effects of intraluminal injection of bone marrow-derived cells (BMC) into experimental CTO. METHODS AND RESULTS: CTO were created in the femoral arteries of 43 New Zealand White rabbits using the thrombin injection model. At 12 weeks following CTO creation, 33 rabbits were injected with either cultured BMC (n=19) or control DMEM alone (n=14) directly into the CTO. Ten rabbits were used for cell tracking (seven BMC and three control). BMC labelled with fluorescent Qdot® nanocrystals were identified in the CTO up to one week after injection. Animals were sacrificed at three to five weeks post-treatment and arterial samples were excised for micro-CT imaging and histologic morphometric analysis. There was a significant but modest increase in neovascularisation in BMC-treated arteries compared to controls (7.47±4.75% vs. 4.35±2.97%, p<0.05). However, unexpected intravascular calcification was only detected within the CTO in BMC cell treated arteries. Western blot for conditioned medium from BMC showed up-regulation of osteogenic proteins (BMP-2 and -7). CONCLUSIONS: Although direct delivery of BMC into CTO increases neovascularisation, undesirable vascular calcification will limit this therapeutic approach.

Heparan sulfate side chains have a critical role in the inhibitory effects of perlecan on vascular smooth muscle cell response to arterial injury.

Perlecan is a proteoglycan composed of a 470-kDa core protein linked to three heparan sulfate (HS) glycosaminoglycan chains. The intact proteoglycan inhibits the smooth muscle cell (SMC) response to vascular injury. Hspg2(Δ3/Δ3) (MΔ3/Δ3) mice produce a mutant perlecan lacking the HS side chains. The objective of this study was to determine differences between these two types of perlecan in modifying SMC activities to the arterial injury response, in order to define the specific role of the HS side chains. In vitro proliferative and migratory activities were compared in SMC isolated from MΔ3/Δ3 and wild-type mice. Proliferation of MΔ3/Δ3 SMC was 1.5× greater than in wild type (P < 0.001), increased by addition of growth factors, and showed a 42% greater migratory response than wild-type cells to PDGF-BB (P < 0.001). In MΔ3/Δ3 SMC adhesion to fibronectin, and collagen types I and IV was significantly greater than wild type. Addition of DRL-12582, an inducer of perlecan expression, decreased proliferation and migratory response to PDGF-BB stimulation in wild-type SMC compared with MΔ3/Δ3. In an in vivo carotid artery wire injury model, the medial thickness, medial area/lumen ratio, and macrophage infiltration were significantly increased in the MΔ3/Δ3 mice, indicating a prominent role of the HS side chain in limiting vascular injury response. Mutant perlecan that lacks HS side chains had a marked reduction in the inhibition of in vitro SMC function and the in vivo arterial response to injury, indicating the critical role of HS side chains in perlecan function in the vessel wall.

Obesity phenotype and incident hypertension: a prospective community-based cohort study.

OBJECTIVE: The relationship betweens the healthy obese phenotype and the risk of cardiovascular events remains unclear. We prospectively investigated the association between the obesity phenotype and the incidence of hypertension. METHODS: We studied 2352 participants, aged 40-69 years at baseline, with normal blood pressure (BP) from the Ansan cohort and the Ansung cohort of the Korean Genome Epidemiology Study. Participants were divided into six groups based on BMI and the metabolic syndrome (MetS) components: healthy (none of the five MetS components) normal weight (BMI <23 kg/m(2)), unhealthy (one or more MetS component) normal weight, healthy overweight (BMI 23-24.9 kg/m(2)), unhealthy overweight, healthy obesity (BMI ≥25 kg/m(2)), and unhealthy obesity. The incidence of hypertension was identified by biennial health examinations during the 8-year follow-up. RESULTS: After adjusting for age, sex, cohort, physical activity, smoking, alcohol consumption, and family history of hypertension and cardiovascular diseases, an increased risk for hypertension in combined cohort was observed in the healthy obesity [hazard ratio (HR): 2.20, 95% confidence interval (CI):1.34-3.60], unhealthy overweight (HR: 1.47, 95% CI: 1.00-2.14), and unhealthy obesity (HR: 2.45, 95% CI: 1.79-3.37), compared with the healthy normal weight group. In each cohort, the healthy obesity was still associated with a higher incidence of hypertension (HR 2.20, 95% CI 1.11-4.36 for the Ansan cohort and HR 2.21, 95% CI 1.01-4.83 for the Ansung cohort). CONCLUSION: These findings provide evidence that the metabolically healthy obese phenotype may not be a benign condition.

Discordant impairment of multidirectional myocardial deformation in rats with Doxorubicin induced cardiomyopathy.

BACKGROUND: In doxorubicin-induced cardiomyopathy (DIC), the sequence of decrease in multidirectional myocardial deformation has not been clearly elucidated. OBJECTIVES: We investigated the sequence of myocardial deformations in rat DIC, using two-dimensional speckle tracking echocardiography (2DSTE). METHODS: Twenty rats were treated with doxorubicin (1.25 mg/kg × 16 times, intraperitoneal) for 4 weeks and compared with nine control rats. Myocardial strain analysis with 2DSTE, as well as conventional echocardiography, was obtained. RESULTS: Compared with baseline, longitudinal strain/strain rate (LS/LSr) decreased at week 2 (-15.7 ± 1.5 to -14.1 ± 1.4%, P = 0.01 for LS; -4.4 ± 0.7 to -3.9 ± 0.5 per second, P = 0.009 for LSr). Left ventricular ejection fraction (LVEF) and circumferential strain (CS) decreased at week 4 (80.3 ± 3.2 to 78.1 ± 3.3%, P = 0.031 for LVEF; -18.6 ± 1.9 to -15.0 ± 3.4%, P = 0.019 for CS). Circumferential strain rate (CSr) decreased at week 6 (-5.5 ± 0.8 to -4.6 ± 1.0 per second, P = 0.008). Radial strain/strain rate (RS/RSr) decreased at week 8 (54.8 ± 9.4 to 43.7 ± 10.6%, P = 0.005 for RS; 8.0 ± 1.1 to 7.0 ± 1.1 per second, P = 0.005 for RSr), while there was no significant change in LS/LSr, LVEF, CS/CSr, or RS/RSr in the control group. LVEF had the highest correlation with LS (r =-0.607, P = 0.000) and the lowest correlation with RSr (r = 0.357, P = 0.000). CONCLUSIONS: In DIC of rat hearts, LS/LSr decreased first, and then LVEF, CS, CSr, RS/RSr subsequently decreased. LS/LSr is considered to be a more sensitive predictor than LVEF in progressive rat DIC, and RS/RSr was preserved until the last stage.

Primary angiosarcoma of the pulmonary trunk mimicking pulmonary thromboembolism.

We present a case of primary angiosarcoma of the pulmonary trunk that was initially misdiagnosed as a subacute massive pulmonary thromboembolism in a 26-year-old woman. This is an extremely rare disease that is usually indistinguishable from acute or chronic thromboembolic disease of the pulmonary arteries because the clinical and radiologic findings of pulmonary artery angiosarcoma are similar to those of pulmonary thromboembolism. Although the incidence of pulmonary artery angiosarcoma is very low, our case demonstrates that this disease entity should be included in the differential diagnosis of pulmonary thromboembolism, especially in patients who do not respond to anticoagulant therapy or present with no identifiable source of thromboembolic events.

Comparison of effects of telmisartan and valsartan on late lumen loss and inflammatory markers after sirolimus-eluting stent implantation in hypertensive patients.

We compared the effects of telmisartan and valsartan on late lumen loss and inflammatory markers after sirolimus-eluting stent implantation in hypertensive patients. This was a prospective, randomized, single-blinded, 8-month follow-up study that included hypertensive patients with significant coronary artery stenosis treated with telmisartan (n=79) or valsartan (n=80). Risk factors such as diabetes, hyperlipidemia, smoking, and obesity were similar between groups. After 8 months of follow-up, only the telmisartan group showed significant decreases in interleukin-6 and tumor necrosis factor-alpha. The decreases from baseline level in total cholesterol and low-density lipoprotein cholesterol concentrations were significantly greater in the telmisartan group. The increase in adiponectin concentrations from baseline measurements was significantly greater in the telmisartan group than in the valsartan group (1.9+/-2.7 vs 0.4+/-2.0 microg/ml, respectively, p<0.05). Moreover, late lumen loss was significantly lower in the telmisartan group than in the valsartan group (0.1+/-0.4 vs 0.3+/-0.5 mm, respectively, p=0.001). Major adverse cardiac events were similar between groups. In conclusion, compared with valsartan, telmisartan was associated with a significant decrease in late lumen loss and inflammatory markers after sirolimus-eluting stent implantation in hypertensive patients with significant coronary narrowing.

A case of non-functioning huge adrenocortical carcinoma extending into inferior vena cava and right atrium.

Primary adrenocortical carcinoma (ACC) is a rare tumor and its usual sites of metastasis are the lung (71%), lymph node (68%), liver (42%), and bone (26%). However, intracaval invasion extending into the right atrium is very rare and spontaneous regression of tumor burden in adrenal carcinoma is also rare. We report a case of ACC with direct invasion of the inferior vena cava and right atrium. A 34-yr-old male patient presented with progressive dyspnea, weight loss, and poor oral intake over 3 months. Non-functioning ACC with direct invasion of the inferior vena cava and right atrium was confirmed by imaging, pathologic, and hormonal study. Chemo-radiotherapy was attempted. However, tumor burden was not changed, but rather toxic hepatitis and thrombocytopenia were developed. His subjective symptoms and general conditions were improved after 1 month of conservative management and the patient was discharged. During clinical follow-up, this tumor showed spontaneous regression.

Varix of the right atrium.

A 68-year-old female patient was referred for the evaluation of an incidentally detected asymptomatic cardiac mass. Imaging studies showed a 3.0 x 2.4 cm, well circumscribed, round, cystic mass with a calcified nodule that was attached to the lower rim of the fossa ovalis in the right atrium. Under cardiopulmonary bypass, the right atrium was opened to reveal a well circumscribed, dark bluish, pedunculated mass. Histologically, the specimen was a unilocular cyst lined by flattened endothelium, with peripheral fibrin clots and dystrophic calcification of the wall. Immunohistochemical staining of the lining cells was positive for cluster designation 34, which represents hematopoietic progenitor cell antigen. The final pathologic diagnosis was compatible with varix of the heart, which should be considered for a cystic mass with a calcified nodule located in the right atrium, near the lower rim of the fossa ovalis.

The effects of mesenchymal stem cells transduced with Akt in a porcine myocardial infarction model.

OBJECTIVE: This study was designed to examine whether mesenchymal stem cells (MSCs) transduced with Akt enhance cardiac repair after transplantation into the ischemic porcine heart. METHODS: MSCs isolated from porcine bone marrow and transduced with myr-Akt were transplanted into porcine hearts after experimental myocardial infarction (MI) using intracoronary injection [Group I, vehicle; Group II, MSCs; Group III, Akt-MSCs]. Myocardial single photon emission tomography (M-SPECT) was performed to assess myocardial function and the infarcted area. Pigs were also sacrificed for immunohistochemical characterization and histologic analysis. In addition, in vitro assays were performed to examine the resistance of Akt-MSCs to H(2)O(2) stimulation. RESULTS: Transplantation of MSCs into the ischemic porcine myocardium (Group II) increased the left ventricular ejection fraction (DeltaLV EF; -6.3 +/- 15.1% versus 0.5 +/- 6.4%, P < 0.001) and decreased the Deltaarea of MI (6.8+/-5.6% versus -5.0+/-5.3%, P < 0.001) compared with the vehicle control (Group I). Transplantation of MSCs transduced with myr-Akt (Group III) resulted in further improvement in DeltaLV EF (-6.3 +/- 15.1% versus 5.8 +/- 11.3%, P < 0.001) and in Deltaarea of MI (6.8 +/- 5.6% versus -17.0 +/- 7.6%, P < 0.001). Akt-MSCs were more resistant to apoptosis, and the levels of extracellular signal-regulated protein kinase (ERK) activation and vascular endothelial growth factor (VEGF) were higher in H(2)O(2)-stimulated Akt-MSCs. CONCLUSION: Cellular transplantation of Akt-MSCs further enhances the repair of injured myocardium compared to MSC transplantation alone by increasing the number of viable MSCs after cellular transplantation.

Usefulness of physical maneuvers for prevention of vasovagal syncope.

BACKGROUND: It is known that approximately two-thirds of patients with vasovagal syncope have prodromal symptoms and when these start, physical maneuvers that can increase venous return may abort the syncopal attack. The aims of this study were to evaluate the effects of 3 physical maneuvers, squatting, leg-crossing with muscle tensing, and handgrip, on improving hemodynamic status, and to compare the effect of each on aborting or preventing vasovagal syncope. METHODS AND RESULTS: Of 50 patients who underwent the head-up tilt test (HUT) to evaluate syncope, 27 patients with positive HUT were classified as group I (14 men, 13 women; mean age 44.5+/-15.3 years), 23 patients with negative HUT were classified as group II (13 men, 10 women; mean age 41.2 +/-16.7 years), and 21 normal subjects were classified as group III (10 men, 11 women; mean age 28.6+/-6.3 years). The effects of the physical maneuvers were evaluated in 21 patients from group I who underwent a repeat HUT 1 week after the initial test. Leg-crossing significantly increased systolic blood pressure (SBP) in all 3 groups (8.0+/-5.8 mmHg in group I, 7.0+/-8.5 mmHg in group II, 8.7+/-5.7 mmHg in group III; p < 0.05), but not diastolic blood pressure (DBP). Squatting significantly increased SBP and DBP in all 3 groups (7.1 +/-5.1, 4.6+/-5.8 mmHg in group I, 7.8+/-5.9, 4.3+/-4.7 mmHg in group II, 6.5+/-5.0, 3.7+/-3.9 mmHg in group III; p < 0.05). However, handgrip did not exert any significant influence on the hemodynamics in any group nor did heart rate change significantly during the physical maneuvers in any group. During the repeat HUT, prodromal symptoms with hypotension developed in 13 of the 21 patients and of these 5 fainted immediately after and were not able to do the physical maneuvers. Squatting and leg-crossing aborted syncope in 7 of 8 patients, but handgrip aborted syncope in only 1 patient. CONCLUSION: Squatting and leg-crossing with muscle tensing improved the hemodynamics of normal subjects as well as those of patients with vasovagal syncope. Squatting and leg-crossing can be used as a simple and effective preventive maneuver in patients with vasovagal syncope.

Preinterventional peak monocyte count and in-stent intimal hyperplasia after coronary stent implantation in human coronary arteries.

BACKGROUND: The mechanism of restenosis after stent implantation principally is neointimal hyperplasia. There is evidence that monocytes play a important role in in-stent restenosis (ISR) after stent implantation. HYPOTHESIS: This study assessed the relationship between preinterventional peak monocyte count and neointimal growth after successful stent implantation. METHODS: We performed coronary stent implantation in 85 patients (85 de novo lesions). Peripheral blood sample was obtained in all patients every 12 h before coronary angiography for measurement of peripheral monocytes. All patients received angiographic and intravascular ultrasound (IVUS) follow-up at 6 months after stenting. RESULTS: The preinterventional circulating monocyte count was significantly higher in the ISR group than that in the group without ISR (654 +/- 62/vs. 461 +/- 222/mm3, p < 0.001) and was significantly higher in the reintervention group than that in the no-reintervention group (660 +/- 72/ vs. 470 +/- 216/mm3, p< 0.001). The incidence of ISR and repeat intervention associated with preinterventional monocyte count was highest among the patients in the highest tertile, who were at a 2.64-fold increased risk of ISR and 3.22-fold increased risk of repeat intervention compared with the patients in the lowest tertile. A significant positive correlation was found between preinterventional peak monocyte count and preinterventional plaque and media cross-sectional area and follow-up neointima area (r = 0.311, p = 0.007, r = 0.465, p < 0.001, respectively). The neointima area associated with preinterventional monocyte count was largest among the patients in the highest tertile, that is, 2-fold larger than that of the patients in the lowest tertile (p < 0.001) and 1.44-fold larger than that of the patients in the middle tertile (p = 0.001). CONCLUSION: Our results suggest that circulating preinterventional monocytes play a principal role in the process of in-stent neointimal growth after successful stent implantation.

Effect of combined intracoronary adenosine and nicorandil on no-reflow phenomenon during percutaneous coronary intervention.

BACKGROUND: This study aimed to clarify the effect of intracoronary administration of combined adenosine and nicorandil on the no-reflow phenomenon. METHODS AND RESULTS: Fifty patients (67+/-10 years, 30 male) with acute myocardial infarction (AMI) who developed no-reflow phenomenon during primary percutaneous coronary intervention (PCI) between June 2001 and May 2003 comprised the study group, which was divided into 2 groups: group I [25 patients, 67+/-10 years, 13 male; adenosine (24 microg/ml) alone in addition to nitrate] and group II [25 patients, 66+/-9 years, 17 male; combined intracoronary administration of adenosine and nicorandil (2 mg/ml) in addition to nitrate]. In-hospital and 6-month major adverse cardiac events (MACE) after PCI were compared between the 2 groups. Risk factors of coronary disease, left ventricular ejection fraction and wall motion score were not significantly different between the 2 groups (p=NS). Time interval from the onset of chest pain to PCI, number of involved vessels, lesion type according to ACC/AHA classification and TIMI flow grade (TFG) were not significantly different in both groups (p=NS). Incidence of thrombosis or dissection after balloon angioplasty, diameter and length of stent, and use of Reopro during PCI were not significantly different. TFG after PCI (2.0+/-0.9 vs 2.6+/-0.6, p=0.024), DeltaTFG (1.5+/-1.1 vs 2.2+/-1.0, p=0.033) and difference in TIMI frame count (TFC) before and after PCI (DeltaTFC) were greater in group II than group I (45.2+/-24.5 vs 63.6+/-23.2, p=0.014). Myocardial blush score 3 was obtained more frequently in group II than group I (44% vs 76%, p=0.014). In-hospital death did not occur in any of group II, but 4 patients of group I died (p=0.043). Two cases of MACE developed in each group and heart failure occurred in 3 (12%) of group I and 1 (4%) of group II patients during the 6-month follow-up (p=NS). CONCLUSIONS: Intracoronary administration of adenosine combined with nicorandil may improve both the occurrence of no-reflow in patients during PCI for AMI and short-term clinical outcome, compared with adenosine alone.