Association of elevated blood pressure during exercise with cerebral white matter lesions.

OBJECTIVES: Cerebral white matter lesions (WMLs) are regarded to be subclinical ischemic changes of the cerebral parenchyma. Many previous studies have shown that baseline blood pressure (BP) is one of the most important factors for WMLs, but the relation between exercise BP and WMLs has not been fully evaluated. So, we sought to investigate the relationships between cerebral WMLs and peak exercise BP. METHODS: Brain magnetic resonance imaging scan and treadmill testing were performed simultaneously in 130 consecutive subjects without history of stroke or transient ischemic stroke. RESULTS: Among 130 subjects, 42 individuals (32%) presented WMLs. Individuals with WMLs were older than those without WMLs, and baseline systolic BP and pulse pressure were higher in subjects with WMLs. During treadmill test, peak exercise systolic BP was more significantly elevated in subjects with WMLs. In multivariable logistic regression analysis, elevated baseline systolic BP, not peak exercise systolic BP, was associated with the presence of WMLs, independently of age. However, in multivariable logistic regression analysis of 88 normotensive subjects, elevated peak systolic BP during exercise was the only determinant for the presence of WMLs. CONCLUSIONS: Elevated peak systolic BP during exercise is significantly related with WMLs, subclinical small vessel disease of brain, especially in normotensive subjects.

miRNA polymorphisms (miR­146a, miR­149, miR­196a2 and miR­499) are associated with the risk of coronary artery disease.

Small non­coding microRNAs (miRNAs) are not only important for heart and vascular development but are also important in cardiovascular pathophysiology and diseases, such as ischemia and atherosclerosis­related diseases. However, the effect of miR­146a, miR­149, miR­196a2 and miR­499 polymorphisms on coronary artery disease (CAD) susceptibility remain unknown. The aim of the present study was to examine the genotype frequencies of miR­146a, miR­149, miR­196a2 and miR­499 polymorphisms in patients with CAD, and assess their clinical applications for diagnosing and monitoring CAD. Using polymerase chain reaction­amplified DNA, microRNA polymorphisms were analyzed in 522 patients with CAD and 535 control subjects. The miR­149 rs2292832 C>T and miR­196a2 rs11614913 T>C polymorphisms were shown to be significantly associated with CAD prevalence. In subgroup analyses according to disease severity, the miR­146a rs2910164GG genotype was significantly associated with CAD risk in the stent ≥2 group. In addition, miR­146aG/­149T/­196a2C/­499 G allele combination was significantly associated with CAD prevalence (G­T­C­G and G­C­C­G of miR­146a/­149/­196a2/­499). The combination genotypes of miR­146aGG/149TC+CC and miR­149CC/196a2TC were significantly associated with CAD incidence. In subgroup analyses, miR­146a rs2910164 C>G increased the risk of developing CAD in non­smoking, hypertensive and nondiabetic subgroups. Furthermore, miR­149 rs2292832 C>T and miR­196a2 rs11614913 T>C was shown to increase CAD risk in females and patients aged >63 years old. The miR­149T allele, miR­196a2C allele and miR­146aG/­149T/­196a2C/­499 G allele combination were associated with CAD pathogenesis. The combined effects of environmental factor and genotype combination of miRNA polymorphisms may contribute to CAD prevalence.

The additive value of multiple biomarkers in prediction of premature coronary artery disease.

OBJECTIVE: The aim of this study was to determine the value of additional multiple biomarkers in the prediction of premature coronary artery disease (CAD). METHODS AND RESULTS: Data from 503 CAD patients and 503 healthy control patients with matching age and sex were collected. The patient group consisted of male (25 to 55 years) and female (30 to 60 years) patients with documented angiographic multi-vessel CAD. Baseline characteristics of conventional risk factors and biomarkers were collected. We compared the conventional risk factors model with the model with six additional biomarkers (hs-CRP, IL-6, RAGE, Lp-LPA2, adiponectin, and RANTES), which have shown significant association with premature CAD. We also evaluated the effects of adding each of the six biomarkers to the conventional laboratory data. The additional biomarkers model resulted in improvements in the C-statistic (0.953 vs. 0.937, P=0.0003) in comparison with the conventional risk factors model. Among the 6 biomarkers added to the patient group, hs-CRP and IL-6 had a significant discriminative power to predict the risk of premature CAD (hs-CRP; P = 0.0005, IL-6; P= 0.003). CONCLUSIONS: Although conventional risk factors were more strongly associated with premature CAD than were biomarkers, adding the 6 biomarkers (hs-CRP, IL-6, RAGE, Lp-LPA2, adiponectin, and RANTES) improved the prediction of premature CAD moderately. We found that hs-CRP and IL-6 had shown a significant contribution in the prediction of premature CAD.

Association of insulin resistance and coronary artery remodeling: an intravascular ultrasound study.

BACKGROUND: There are few studies that investigated the correlation between insulin resistance (IR) and the coronary artery remodeling. The aim of the study is to investigate the association of IR measured by homeostasis model assessment of insulin resistance (HOMA-IR) and coronary artery remodeling evaluated by intravascular ultrasound (IVUS). METHODS: A total of 298 consecutive patients who received percutaneous coronary interventions under IVUS guidance were retrospectively enrolled. The value of HOMA-IR more than 2.5 was considered as IR positive. Metabolic syndrome was classified according to NCEP ATP III guidelines. The remodeling index was defined as the ratio of the external elastic membrane (EEM) area at the lesion site to the EEM area at the proximal reference site. RESULTS: A total of 369 lesions were analyzed (161 lesions in HOMA-IR positive and 208 lesions in HOMA-IR negative). Remodeling index was significantly higher in the HOMA-IR positive group compared with the negative group (HOMA-IR positive vs. negative: 1.074 ± 0.109 vs. 1.042 ± 0.131, p = 0.013). There was a significant positive correlation between remodeling index and HOMA-IR (p = 0.010). Analysis of HOMA-IR according to remodeling groups showed increasing tendency of HOMA-IR, and it was statistically significant (p = 0.045). Multivariate analysis revealed that only HOMA-IR was an independent predictor of remodeling index (r = 0.166, p = 0.018). CONCLUSION: Increased IR estimated by HOMA-IR was significantly associated with a higher remodeling index and positive coronary artery remodeling.

An exaggerated blood pressure response to exercise is associated with subclinical myocardial dysfunction in normotensive individuals.

OBJECTIVES: An exaggerated blood pressure (BP) response to exercise is associated with adverse cardiovascular outcomes, even in normotensive individuals. The purpose of this study was to compare myocardial function between normotensive individuals with and without an exaggerated BP response. METHODS: We evaluated global myocardial function using speckle tracking echocardiography in normotensive individuals. Two-dimensional speckle tracking echocardiography and a treadmill exercise test were performed simultaneously in 171 normotensive individuals (mean age: 48 ±â€Š8 years; 97 men) without any structural heart disease. RESULTS: Among 171 normotensive individuals, 19 (11%) exhibited an exaggerated BP response (≥200  mmHg for men and ≥190  mmHg for women) during the treadmill test. Conventional echocardiographic parameters were similar between the two groups. However, on strain analyses, the systolic and early diastolic global longitudinal strains of the left ventricle (LV) and left atrium were lower in individuals with an exaggerated BP response to exercise. The peak SBP during exercise was inversely related to systolic global longitudinal strain of the LV (r = -0.35, P < 0.01) and left atrium (r = -0.41, P < 0.01). On multivariate analyses, an exaggerated BP response to exercise was shown to be an independent determinant of reduced global longitudinal strain of the LV (ß = -0.20, P < 0.05) and left atrium (ß = -0.28, P < 0.05). CONCLUSION: Normotensive individuals with an exaggerated BP response to exercise exhibit impairment in longitudinal myocardial function. Even without apparent hypertension, an exaggerated BP response could cause repeated increases in afterload and result in subclinical myocardial dysfunction.

Abolished ischemic tricuspid regurgitation by revascularization of left anterior descending artery: The role of collateral circulation.

A 74-year-old man presented with recent inferior wall myocardial infarction. The right ventricle (RV) was strikingly dilated and akinetic along the free wall compatible with right ventricular infarction. Accordingly, severe functional tricuspid regurgitation (TR) was detected. Coronary angiogram revealed total occlusion on the proximal right coronary artery (RCA). There was collateral blood flow from the left anterior descending (LAD) artery to the right ventricular ischemic region. The LAD artery also had a significant stenosis which might limit the required amount of blood supply to collateral blood vessels. Because of the technical difficulty in the intervention of RCA, the patient underwent percutaneous intervention on the LAD artery. After the revascularization of LAD artery, severe TR was abolished accompanied by the right ventricular functional recovery. .

Extent of late gadolinium enhancement on cardiovascular magnetic resonance imaging and its relation to left ventricular longitudinal functional reserve during exercise in patients with hypertrophic cardiomyopathy.

BACKGROUND: The aim of this study was to investigate whether the extent of late gadolinium enhancement (LGE) on cardiovascular magnetic resonance imaging reflecting myocardial fibrosis correlates with left ventricular (LV) longitudinal function during exercise in hypertrophic cardiomyopathy (HCM). METHODS AND RESULTS: Mitral annular velocities (E' and S') were measured on echocardiography at rest and during graded bicycle exercise (25 W, 3-min increments) in 46 HCM patients (mean age, 53 years; 32 men). LV longitudinal diastolic and systolic functional reserve indices were calculated as ΔE'×E'base and ΔS'×S'base, where ΔE' and ΔS' are the changes in E' and S' from baseline to 50 W of exercise, respectively. The patients were divided into 2 groups according to the extent of LGE (as "percentage of LV mass containing LGE": %LV with LGE; range, 0-37%; median, 6%): group 1 (n=23), %LV with LGE <6%, and group 2, %LV with LGE ≥6%. Baseline echocardiographic parameters were similar between the 2 groups, but changes in E' and S' during exercise were smaller in group 2 (ΔE': 2.8±1.8 cm/s vs.1.5±1.0 cm/s, P=0.007; ΔS': 2.2±1.2 cm/s vs. 0.9±0.8 cm/s, P<0.0001). LV functional reserve indices were also significantly lower in group 2 (ΔE'×E'(base): 12.8±7.7 vs. 5.5±3.4, P=0.001; ΔS'×S'(base): 12.6±7.4 vs. 4.7±4.5, P<0.0001). CONCLUSIONS: LV longitudinal function during exercise is influenced by the extent of LGE in HCM. Myocardial fibrosis may represent a pathologic substrate that determines LV functional reserve in patients with HCM.

Fatal delayed coronary artery perforation after coronary stent implantation.

Most type I and II perforations are predominately caused by hydrophilic and stiff wires, often presented in the delayed form, and do not require pericardial drainage or surgical interventions. However, we report a type III delayed coronary artery perforation at the site of stent implantation after intervention without any evidence of immediate perforations. To the best of our knowledge, this is the first case report of angiographic documentation and treatment of delayed coronary perforation at the site of stent, presented as a cardiac arrest.

Comparison of the efficacy and safety of fixed-dose amlodipine/losartan and losartan in hypertensive patients inadequately controlled with losartan: a randomized, double-blind, multicenter study.

BACKGROUND: Fixed-dose combination drugs may enhance blood pressure (BP) goal attainment through complementary effects and reduced side effects, which leads to better compliance. OBJECTIVE: This study aimed to evaluate the efficacy and safety profiles of once-daily combination amlodipine/losartan versus losartan. METHODS: This was an 8-week, double-blind, multicenter, randomized phase III study conducted in outpatient hospital clinics. Korean patients with essential hypertension inadequately controlled on losartan 100 mg were administered amlodipine/losartan 5 mg/100 mg combination versus losartan 100 mg. The main outcome measures were changes in sitting diastolic blood pressure (DBP) and sitting systolic blood pressure (SBP) and BP response rate from baseline values, which were assessed after 4 and 8 weeks of treatment. Safety and tolerability were also assessed. RESULTS: At week 8, both groups achieved significant reductions from baseline in DBP (11.7 ± 7.0 and 3.2 ± 7.9 mmHg), which was significantly greater in the amlodipine/losartan 5 mg/100 mg combination (n = 70) group (p < 0.0001). Additionally, the amlodipine/losartan 5 mg/100 mg combination group achieved significantly greater reductions in SBP at week 8 and in SBP and DBP at week 4 compared with the losartan 100 mg (n = 72) group (all p < 0.0001). Response rates were significantly higher in the amlodipine/losartan 5 mg/100 mg group versus the losartan 100 mg group (81.4% vs 63.9% at week 4, p < 0.0192; 90.0% vs 66.7% at week 8, p < 0.001). Both treatments were generally well tolerated. CONCLUSION: Switching to a fixed-dose combination therapy of amlodipine/losartan 5 mg/100 mg was associated with significantly greater reductions in BP and superior achievement of BP goals compared with a maintenance dose of losartan 100 mg in Korean patients with essential hypertension inadequately controlled on losartan 100 mg. CLINICAL TRIAL REGISTRATION: Registered at Clinicaltrials.gov as NCT00940680.

Evaluation of the dose-response relationship of amlodipine and losartan combination in patients with essential hypertension: an 8-week, randomized, double-blind, factorial, phase II, multicenter study.

BACKGROUND: Despite recommendations for more intensive treatment and the availability of several effective treatments, hypertension remains uncontrolled in many patients. OBJECTIVE: The aim of this study was to determine the dose-response relationship and assess the efficacy and safety of amlodipine or losartan monotherapy and amlodipine camsylate/losartan combination therapy in patients with essential hypertension. METHODS: This was an 8-week, randomized, double-blind, factorial design, phase II, multicenter study conducted in outpatient hospital clinics among adult patients aged 18-75 years with essential hypertension. At screening, patients received placebo for 2-4 weeks. Eligible patients (n=320) were randomized to one of eight treatment groups: amlodipine 5 mg or 10 mg, losartan 50 mg or 100 mg, amlodipine camsylate/losartan 5 mg/50 mg, 5 mg/100 mg, 10 mg/50 mg, or 10 mg/100 mg. MAIN OUTCOME MEASURES: The assumption of strict superiority was estimated using the mean change in sitting diastolic blood pressure (DBP) at 8 weeks. Safety was monitored through physical examinations, vital signs, laboratory test results, ECG, and adverse events. RESULTS: The reduction in DBP at 8 weeks was significantly greater in patients treated with the combination therapies compared with the respective monotherapies for all specified comparisons except amlodipine camsylate/losartan 10 mg/100 mg versus amlodipine 10 mg. The incidence of adverse events in the group of patients treated with the amlodipine camsylate/losartan 10 mg/50 mg combination tended to be higher than for any other group (27.9%, 12/43); however, the effect was not statistically significant. CONCLUSION: Combination amlodipine camsylate/losartan (5 mg/50 mg, 5 mg/100 mg and 10 mg/50 mg) resulted in significantly greater BP lowering compared with amlodipine or losartan monotherapy, and was determined to be generally safe and tolerable in patients with essential hypertension. CLINICAL TRIAL REGISTRATION: Registered at clinicaltrials.gov: NCT00942344.

Comparison of outcomes of patients with painless versus painful ST-segment elevation myocardial infarction undergoing percutaneous coronary intervention.

There are few data available on the prognosis of painless ST-segment elevation myocardial infarction (STEMI). The aim of this study was to determine the incidence, clinical characteristics, and outcomes of painless STEMI. We analyzed the Korea Acute Myocardial Infarction Registry (KAMIR) study, which enrolled 7,288 patients with STEMI (61.8 ± 12.8 years old, 74% men; painless STEMI group, n = 763; painful STEMI group, n = 6,525). End points were in-hospital mortality and 1-year major adverse cardiac events (MACEs). Patients with painless STEMI were older and more likely to be women, nonsmokers, diabetic, and normolipidemic and to have a higher Killip class. The painless group had more in-hospital deaths (5.9% vs 3.6%, p = 0.026) and 1-year MACEs (26% vs 19%, p = 0.002). In Cox proportional hazards analysis, hypotension (hazard ratio [HR] 4.40, 95% confidence interval [CI] 1.41 to 13.78, p = 0.011), low left ventricular ejection fraction (HR 3.12, 95% CI 1.21 to 8.07, p = 0.019), and a high Killip class (HR 3.48, 95% CI 1.19 to 10.22, p = 0.023) were independent predictors of 1-year MACEs in patients with painless STEMI. In conclusion, painless STEMI was associated with more adverse outcomes than painful STEMI and late detection may have contributed significantly to total ischemic burden. These results warrant more investigations for methodologic development in the diagnosis of silent ischemia and painless STEMI.

Comparative efficacy and safety profile of amlodipine 5 mg/losartan 50 mg fixed-dose combination and amlodipine 10 mg monotherapy in hypertensive patients who respond poorly to amlodipine 5 mg monotherapy: an 8-week, multicenter, randomized, double-blind phase III noninferiority study.

BACKGROUND: The number of hypertensive patients achieving treatment targets is not ideal with therapies that engage a single mechanism of action, and combination therapies using different mechanisms of action can increase drug efficacy in a synergistic way. OBJECTIVE: This noninferiority study compared the clinical efficacy and safety profile of fixed-dose combination of amlodipine/losartan 5/50 mg and amlodipine 10 mg monotherapy in essential hypertensive patients who respond poorly to amlodipine 5 mg monotherapy. METHODS: This was a double-blind, multicenter, randomized trial of hypertensive patients (N = 185) aged ≥18 years taking amlodipine 5 mg during the run-in treatment period but failed to achieve sitting diastolic blood pressure (DBP) <90 mm Hg. After randomization into the amlodipine/losartan 5/50 mg fixed-dose combination group (n = 92) and the amlodipine 10 mg monotherapy group (n = 93), treatment was maintained without dose escalation for 8 weeks. The noninferiority margin was prespecified as 4 mm Hg after 8 weeks of treatment for the difference of the average change in DBP between treatments. The primary efficacy evaluation of noninferiority was tested using a confidence interval approach with a 97.5% 1-sided lower confidence limit using the average difference in DBP measured at baseline and 8 weeks. RESULTS: After 8 weeks, the DBP of both groups decreased from baseline by 8.9 (6.1) and 9.4 (7.5) mm Hg, respectively (difference = -0.5 [6.9] mm Hg, 95% CI: -2.5 to 1.5). Secondary end points of reductions in DBP after 4 weeks (-8.1 [6.7] vs -9.9 [7.3] mm Hg, difference = -1.8 mm Hg, 95% CI: -3.9 to 0.2) and sitting systolic blood pressure after 4 (-10.2 [11.8] vs -12.8 [10.2] mm Hg, difference = -2.6 mm Hg, 95% CI: -5.9 to 0.6) and 8 weeks (-12.2 [11.0] vs -13.4 [11.3] mm Hg, difference = -1.2 mmHg, 95% CI: -4.4 to 2.1) were comparable between the 2 treatment groups. There were 38 adverse events in 20 patients (21.7%) in the amlodipine/losartan 5/50 mg fixed-dose combination group and 31 in 24 patients (26.1%) in the amlodipine 10 mg monotherapy group; most were mild. There were 7 adverse events in 6 patients (6.5%) related to treatment in the fixed-dose combination group and 13 in 10 patients (10.9%) in the monotherapy group (P = 0.30). CONCLUSIONS: Fixed-dose combination amlodipine/losartan 5/50 mg was not inferior in terms of reductions in DBP after 8 weeks of treatment and had comparable safety profile to amlodipine 10 mg in patients who did not respond to amlodipine 5 mg monotherapy. ClinicalTrials.gov identifier: NCT00940667.

Clinical and echocardiographic predictors of outcomes in patients with apical hypertrophic cardiomyopathy.

Apical hypertrophic cardiomyopathy (HC) is considered to have a favorable prognosis, but recent observations have suggested less benign clinical courses. We investigated the outcomes in patients with apical HC and evaluated the predictors. All 454 patients with apical HC (316 men, age 61 ± 11 years) were recruited. Major cardiovascular events (MACE) were defined as unplanned hospitalization because of heart failure, stroke, or cardiovascular mortality. The patients were divided into 2 groups: group 1 with MACE and group 2 without MACE. During the follow-up period (43 ± 20 months), the all-cause mortality rate was 9% (39 of 454), and 110 patients (25%) had MACE. The subjects in group 1 were older and a greater proportion had diabetes, hypertension, and atrial fibrillation. On the echocardiogram, the left atrial volume index (left atrial volume index 36 ± 17 vs 31 ± 12 ml/m(2)), transmitral E velocity (65 ± 17 vs 61 ± 16 cm/s), mitral annulus Ea velocity (4.5 ± 1.4 vs 5.1 ± 1.8 cm/s), Sa velocity (5.8 ± 1.4 vs 6.6 ± 1.4 cm/s), E/Ea ratio (15 ± 5 vs 13 ± 5), and right ventricular systolic pressure (31 ± 8 vs 28 ± 7 mm Hg) were significantly different between groups 1 and 2 (p <0.05 for all). The left atrial volume index (for each 1-ml/m(2) increase, hazard ratio 1.01, 95% confidence interval 1.00 to 1.03; p = 0.047), Sa velocity (hazard ratio 0.83, 95% confidence interval 0.72 to 0.96, p = 0.014), and E/Ea ratio (hazard ratio 1.04, 95% confidence interval 1.00 to 1.09, p = 0.030) were independent predictors of a poor prognosis, along with age and the presence of diabetes or hypertension. In conclusion, the clinical outcomes of patients with apical HC were less benign in older patients and in those with hypertension or diabetes. In addition, the left atrial volume index, Sa velocity, and E/Ea ratio were predicters of a poor prognosis in patients with apical HC.

Vena contracta width as a predictor of adverse outcomes in patients with severe isolated tricuspid regurgitation.

BACKGROUND: The clinical outcomes and predictors of outcomes in isolated tricuspid regurgitation (TR) are poorly defined. The aim of this study was to investigate the determinants of outcomes in severe isolated TR. METHODS: Seventy-four patients (mean age, 63 ± 12 years; 34 men) with severe isolated TR who satisfied the criteria of (1) TR jet area > 30% of right atrial area or TR jet area > 10 cm(2) and (2) a plethora of inferior vena cava or systolic flow reversal of the hepatic vein were retrospectively analyzed. The primary end points were hospitalization for worsening heart failure, tricuspid valve (TV) surgery, and cardiovascular death. RESULTS: During the median follow-up period of 53 months, 25 events occurred (three cardiovascular deaths, nine TV surgeries, and 13 hospitalizations for worsening heart failure). Univariate Cox analysis showed that younger age, female gender, larger effective regurgitant orifice, vena contracta width (VCW), and increased right atrial and right ventricular size were associated with cardiovascular events. Increased TV tethering distance and tethering area were also associated with cardiovascular events. In multivariate Cox regression analysis, larger VCW (hazard ratio, 1.72; 95% confidence interval, 1.15-2.57, P < 0.01) was an independent predictor of cardiovascular events. Compared with patients with VCW ≤ 7 mm, those with VCW > 7 mm had poorer long-term outcomes (adjusted hazard ratio, 19.9; P < .01). Increased VCW was also an independent predictor of cardiovascular death and TV surgery (hazard ratio, 1.2; 95% confidence interval, 1.00-1.45; P = .04). CONCLUSIONS: In severe isolated TR, VCW is a powerful independent predictor of adverse outcomes. Adverse outcomes were considerable for VCW > 7 mm, which suggests that quantification of TR by Doppler echocardiography is crucial for estimating prognosis. TV surgery might be considered for patients with severe isolated TR with VCW > 7 mm.

Percutaneous cardiopulmonary support-supported percutaneous coronary intervention: a single center experience.

BACKGROUND AND OBJECTIVES: Percutaneous cardiopulmonary support (PCPS) has proven to be a valuable technique in high-risk coronary patients undergoing percutaneous coronary intervention (PCI). However, there have been few studies on PCI associated with PCPS in Korea. We summarized our experience with PCPS-supported PCI. SUBJECTS AND METHODS: We retrospectively reviewed 19 patients with PCPS-supported PCI between August 2005 and June 2009. PCPS was used as an elective procedure for 10 patients with at least two of the following conditions: left-ventricular ejection fraction <35%, target vessel(s) supplying more than 50% of the viable myocardium, high risk surgical patients, and patients who refused coronary bypass surgery. In the remaining 9 patients PCPS was used as an emergency procedure, to stabilize and even resuscitate patients with acute myocardial infarction and cardiogenic shock, in order to attempt urgent PCI. RESULTS: Among the 19 patients who were treated with PCPS-supported PCI, 11 (57.9%) survived and 8 (42.1%) patients did not. ST elevation myocardial infarction with cardiogenic shock was more prevalent in the non-survivors than in the survivors (75% vs. 27.3%, p=0.04). The elective PCPS-supported PCI was practiced more frequently in the survivors than in the non-survivors (72.7% vs. 25%, p=0.04). In the analysis of the event-free survival curve between elective and emergency procedures, there was a significant difference in the survival rate (p=0.025). Among the survivors there were more patients with multi-vessel disease, but a lower Thrombolysis in Myocardial Infarction grade in the culprit lesions was detected in the non-survivors, before PCI. Although we studied high-risk patients, there was no procedure-related mortality. CONCLUSION: Our experience suggests that PCPS may be helpful in high risk patients treated with PCI, especially in elective cases. More aggressive and larger scale studies of PCPS should follow.

What is optimal revascularization strategy in patients with multivessel coronary artery disease in non-ST-elevation myocardial infarction? Multivessel or culprit-only revascularization.

BACKGROUND: In patients with non-ST-elevation myocardial infarction (NSTEMI), current guidelines did not recommend optimal revascularization management in multivessel coronary artery disease. We compared clinical outcomes between multivessel revascularization and culprit-only revascularization in this setting. METHODS: A total of 1919 patients with multivessel disease (1011 patients; multivessel revascularization group, 908 patients; culprit-only revascularization group) diagnosed as NSTEMI was enrolled in a nationwide prospective Korea Acute Myocardial Infarction Registry (KAMIR) from November 2005 to January 2008. The primary end-points were major adverse cardiac events (MACE), all-causes of deaths, myocardial infarction (MI), and repeated percutaneous coronary intervention (PCI) during 1-year clinical follow-up. Also, subgroup analysis was performed in patients with high TIMI (Thrombolysis In Myocardial Infarction) risk score (≥ 4) to find efficacy of multivessel PCI in high-risk patients. RESULTS: Baseline clinical characteristics and the risk factors of coronary artery disease were similar between both groups. In angiography, three-vessel lesion was more presented in the multivessel group (46.1% vs. 40.9%, p = 0.024) and rates of left anterior descending and left main stem coronary artery as culprit vessel were higher in the multivessel group (p = 0.003 and p = 0.001 respectively). In-hospital mortality was higher in the culprit-only group (1.4% vs. 2.9%, p = 0.025). Primary end-points occurred in 241 patients (15.5%) during 1-year follow-up. Multivessel revascularization reduced MACEs [hazard ratio (HR) 0.658, 95% confidence interval (CI) 0.45 to 0.96, p = 0.031], death or myocardial infarction (HR 0.58, 95% CI 0.35 to 0.97, p = 0.037) and non-target vessel revascularization (HR 0.44, 95% CI 0.24 to 0.81, p = 0.008). There were no significant differences in target lesion revascularization (TLR; HR 1.38, 95% CI 0.51 to 3.71, p = 0.529) and target vessel revascularization (TVR; HR 0.28, 95% CI 0.05 to 1.47, p = 0.131). In subgroup analysis in patients with a higher TIMI risk score, similar results were presented. CONCLUSION: Multivessel revascularization in multivessel coronary artery disease presenting with NSTEMI showed better clinical outcomes without significant in-stent restenosis and progression of diseased-vessel compared to culprit-only revascularization.

Vascular endothelial growth factor, soluble fms-like tyrosine kinase 1, and the severity of coronary artery disease.

BACKGROUND: The association between vascular endothelial growth factor (VEGF), soluble fms-like tyrosine kinase 1 (sFlt-1), and coronary artery disease (CAD) was investigated. METHODS: We enrolled 112 hypertensive patients with proven CAD and 112 hypertensive controls matched for age and gender. The severity of CAD was assessed by the most severe clinical presentation of CAD in patients' history and by the number of diseased vessels. RESULTS: Vascular endothelial growth factor level was lower, whereas sFlt-1 level was higher in the CAD group compared to the controls. Diabetes mellitus (P = .001), smoking (P = .004), and higher sFlt-1 level (P = .01) were independently associated with CAD. Younger age (P = .02), smoking (P = .049), and higher VEGF levels (P = .02) were independently associated with a history of myocardial infarction (MI), whereas higher sFlt-1 level (P = .01) was independently associated with multivessel disease. CONCLUSION: Plasma sFlt-1 levels are positively associated with the presence of CAD and are associated with angiographical severity of CAD.

Incidence and natural history of coronary artery aneurysm developing after drug-eluting stent implantation.

AIMS: There is a growing concern about the occurrence of coronary artery aneurysms (CAAs) after drug-eluting stent (DES) implantation and their long-term course. We assessed the occurrence and the factors affecting the long-term outcome of DES-associated CAA. METHODS AND RESULTS: We analyzed 3,612 consecutive patients (4,419 lesions) who underwent follow-up angiography after DES implantation. All 34 CAAs (0.76% per lesion) in 29 patients (0.8% per patient) were detected at follow-up, and the mean elapsed time from DES implantation to CAA diagnosis was 414 ± 213 days. Angiographically, CAAs developed almost exclusively in complex (type B2/C) de novo lesions (30 [88.2%] of 34 lesions), and lesion length was significantly greater in patients with CAA than without CAA (26.9 ± 9.03 vs 23.1 ± 7.14 mm; P = .004). Myocardial infarction with stent thrombosis occurred in 5 patients with CAA (17.2%), 4 of whom were on aspirin only without clopidogrel. CONCLUSION: Although CAAs rarely develop after DES implantation and show mostly favorable clinical courses, long-term maintenance of clopidogrel therapy might be required to minimize occurrence of adverse clinical events resulting from stent thrombosis.

Dyssynchronous systolic expansion of carotid artery in patients with marfan syndrome.

BACKGROUND: Marfan syndrome is a multisystemic connective tissue disorder associated with a mutation affecting fibrillin-1, the main component of microfibrils. Fibrillin-1 gene mutations may affect the carotid arterial wall. The aim of this study was to investigate carotid arterial mechanics using Velocity Vector Imaging (VVI) in patients with Marfan syndrome. METHODS: Forty-five patients (26 men; mean age, 39 ± 10 years) with Marfan syndrome who fulfilled the Ghent criteria and 45 gender-matched and age-matched healthy volunteers were evaluated. Transverse images of right common carotid artery proximal to the bifurcation were obtained for each subject and divided into six segments. The peak radial velocity, circumferential strain, and strain rate of the six segments were analyzed using VVI. The time to peak radial velocity (T(s)), peak circumferential strain (T(st)), and peak strain rate (T(sr)) of the six segments were calculated. Intima-media thickness was measured for each subject. RESULTS: The average diameter of the common carotid artery in patients with Marfan syndrome was significantly larger than that of controls. Carotid compliance coefficients and distensibility coefficients as assessed by B-mode echocardiographic images were comparable between the two groups. In VVI analyses, averages and standard deviations of peak radial velocities, circumferential strain, and strain rates were not significantly different between the two groups. However, T(s), T(st), and T(sr) were more delayed (P < .01), and the standard deviations of T(s), T(st), and T(sr) were significantly larger in patients with Marfan syndrome (P = .01, P < .01, and P < .01, respectively), suggesting delayed and dyssynchronous arterial expansion during systole. The presence of Marfan syndrome was independently and significantly related to increased standard deviations of T(st) (ß = 0.33, P < .01) and T(sr) (ß = 0.44, P < .01), even after adjusting for age in multiple regression analysis. CONCLUSION: In patients with Marfan syndrome, carotid arteries assessed with VVI exhibited delayed, dyssynchronous arterial expansion during systole compared with healthy controls. Arterial assessment using VVI may be useful for noninvasively quantifying vascular alterations associated with Marfan syndrome.