Detection of increased temperature of the culprit lesion after recent myocardial infarction: the favorable effect of statins

Background

Increased thermal heterogeneity has been demonstrated in atherosclerotic plaques, with the higher temperature recorded in acute myocardial infarction (MI). Dietary or treatment interventions reduce heat production. The purpose of the present study was to investigate whether increased plaque temperature is maintained for a prolonged period after MI and the role of statin administration.

Methods

We enrolled 55 patients, 29 with recent MI and 26 with chronic stable angina (CSA). Total cholesterol, C-reactive protein (CRP), interleukin-6 (IL-6) and soluble adhesion molecules were measured in the study population. All patients underwent coronary plaque temperature measurements. Temperature difference (ΔT) was designated as the temperature of the culprit atherosclerotic plaque minus the temperature of the proximal healthy vessel wall.

Results

Under treatment with statins were 19 patients with recent MI and 14 with CSA. In patients with recent MI ΔT was 0.19 ± 0.18°C, while in patients with CSA was 0.10 ± 0.08°C (P = .03). Patients treated with statins had lower ΔT compared to untreated patients (0.10 ± 0.11 versus 0.20 ± 0.18°C, P = .01). Treated patients with recent MI had similar ΔT compared to CSA patients treated with statins (0.13 ± 0.13 versus 0.07 ± .06° C, P = .14), while untreated patients with recent MI had substantially increased ΔT compared to untreated patients with CSA (0.28 ± 0.22 versus 0.14 ± 0.10°C, P = .04). ΔT was positively correlated with CRP (R = 0.50, P < .01), IL-6 (R = 0.58, P < .01), and intercellular adhesion molecule-1 (R = 0.40, P = .03) levels.

Conclusion

Increased plaque temperature is observed for an extended period after myocardial infarction, indicating that the inflammatory process is sustained after plaque rupture. Statins have a beneficial effect after MI on plaque temperature.     

Randomized comparison of direct stenting with predilatation followed by stenting on vessel trauma and restenosis

Background

Direct stenting may reduce trauma to the vessel wall, thereby having a positive impact on acute and long-term results. This study evaluated acute vessel trauma and acute and follow-up angiographic and intravascular ultrasound (IVUS) results after direct stenting in comparison to conventional stenting.

Methods

Two hundred forty-nine patients were randomly assigned to direct stenting (n = 124) or stenting after predilatation (n = 125) and were followed up by angiography at 6 ± 2 months. Intracoronary serum endothelin (ET-1) levels were determined distal to the lesion before and after coronary intervention to define vessel trauma, and IVUS was performed before and after intervention and at follow-up to determine induced changes in vessel morphology and intimal hyperplasia in a subgroup of 40 patients.

Results

Feasibility of direct stenting was 91%, with 9% requiring crossover to predilatation. There were no differences between the 2 groups in immediate clinical, angiographic, and intravascular ultrasound results. Intracoronary ET-1 levels increased significantly after intervention, without differences between the 2 groups (increase in ET-1 level, 0.79 ± 1.06 vs 0.96 ± 1.22 fmol/L, P = .206). At 6-month follow-up, angiographic late loss (0.76 ± 0.86 vs 0.69 ± 1.09 mm, P = .788) and restenosis rate (21% vs 20%, P = 1.000) were similar for direct stenting versus conventional stenting, respectively. IVUS demonstrated comparable intimal hyperplasia areas for direct versus conventional stenting (2.0 ± 1.5 mm² vs 2.2 ± 1.6 mm², respectively, P = .243).

Conclusions

Direct stenting is highly feasible and results in similar vessel trauma and change in vessel morphology and acute lumen dimensions compared with stenting after predilatation. Similar acute angiographic and IVUS results persist at 6-month follow-up.     

Oxidized low-density lipoprotein levels circulating in plasma and deposited in the tissues: comparison between Helicobacter pylori-associated gastritis and acute myocardial infarction

Background

Oxidized low-density lipoprotein (ox-LDL) is a key factor in the progression of atherosclerosis. We developed a sensitive method for measuring plasma ox-LDL levels using a novel anti-ox-LDL antibody. Recently, several studies have shown positive associations between Helicobacter pylori (H pylori) infection and coronary heart disease. Thus the question arises whether an increase in the plasma levels of ox-LDL occurs in patients with H pylori gastritis.

Methods

We measured plasma ox-LDL levels in patients with H pylori gastritis (n = 27) and compared them with those in patients with acute myocardial infarction (AMI) (n = 62) and stable angina pectoris (SAP; n = 63) and those in control subjects (n = 64). In addition, ox-LDL localization and the presence of macrophages and neutrophils were studied immunohistochemically in gastritis specimens and in coronary culprit lesions obtained from patients with AMI.

Results

Plasma ox-LDL levels in patients with AMI were significantly higher than those in patients with SAP (P <.0001), patients with H pylori gastritis (P <.0001), or in control subjects (P <.0001; AMI, 1.34 ± 0.95; SAP, 0.61 ± 0.29; Gastritis, 0.53 ± 0.17; control, 0.57 ± 0.23 ng/5μg LDL protein). Immunohistochemically, H pylori gastritis specimens showed distinct infiltration of macrophages and myeloperoxidase-positive neutrophils; however, ox-LDL localization was not detected. In contrast, coronary culprit plaques revealed strong positivity for ox-LDL in ruptured lipid cores with abundant macrophage-derived foam cells, and these plaques also contained myeloperoxidase-positive neutrophils.

Conclusion

Our results suggest that plasma ox-LDL levels do not seem to be associated with H pylori infection, but do relate to coronary plaque instability in AMI.     

Myocardial endothelin-1 release and indices of inflammation during angioplasty for acute myocardial infarction and stable coronary artery disease

Background

Elevations in endothelin-1 (ET-1) and inflammatory cytokines may impair myocardial reperfusion through the induction of microvascular constriction or obstruction; however, the generation of these factors close to the site of lesion rupture is unknown.

Methods and results

Coronary sinus (CS) and aortic blood was sampled during angioplasty for acute myocardial infarction (AMI) or stable angina to assess the local release of ET-1, interleukin-1β, interleukin-6, tumor necrosis factor-α and C-reactive protein following atherosclerotic plaque rupture. Transthoracic echocardiography documented left ventricular function in AMI. ET-1 levels were higher in CS than in aortic blood in AMI (3.0 ± 0.3 pmol/L vs 2.6 ± 0.3 pmol/L, P = .04), but not in stable angina (1.7 ± 0.2 pmol/L vs 1.5 ± 0.3 pmol/L, P = NS). CS ET-1 levels were also higher in AMI than in stable angina (3.0 ± 0.3 pmol/L vs 1.7 ± 0.2 pmol/L, P = .002), and correlated with left ventricular dysfunction (R² = 0.51, P = .02). In contrast, C-reactive protein levels were higher in CS than in aortic blood only in stable angina (2.3 ± 0.4 mg/L vs 1.8 ± 0.3 mg/L, P = .01). Similarly, CS tumor necrosis factor-α was higher in stable angina than in AMI (6.0 ± 1.4 pg/mL vs 2.5 ± 0.9 pg/mL, P = .02).

Conclusions

Local myocardial release of ET-1 is highest in AMI, where it relates to the extent of myocardial dysfunction. Although local inflammation is a component of stable coronary artery disease, it does not appear acutely enhanced in AMI.     

Clinical usefulness and prognostic value of elevated cardiac troponin I levels in acute pulmonary embolism

Background

Right ventricular myocardial ischemia and injury contribute to right ventricular dysfunction and failure during acute pulmonary embolism. The objective of this study was to evaluate the clinical usefulness of cardiac troponin I (cTnI) in the assessment of right ventricular involvement and short-term prognosis in acute pulmonary embolism

Methods

Thirty-eight patients with acute pulmonary embolism were included in the study. Clinical characteristics, right ventricular involvement, and clinical outcome were compared in patients with elevated levels of serum cTnI versus patients with normal levels of serum cTnI.

Results

Among the study population (n = 38 patients), 18 patients (47%) had elevated cTnI levels (mean ± SD 1.6 ± 0.7 ng/mL, range 0.7-3.7 ng/mL, median, 1.4 ng/mL), and comprised the cTnI-positive group. In the other 20 patients, the serum cTnI levels were normal (≤0.4 ng/mL), and they comprised the cTnI-negative group. In the cTnI-positive group (n = 18 patients), 12 patients (67%) had right ventricular dilatation/hypokinesia, compared with 3 patients (15%) in the cTnI-negative group (n = 20 patients, P = .004). Right ventricular systolic pressure was significantly higher in the cTnI-positive group (51 ± 8 mm Hg vs 40 ± 9 mm Hg, P = .002). Cardiogenic shock developed in a significantly higher number of patients with elevated serum cTnI levels (33% vs 5%, P = .01). In patients with elevated cTnI levels, the odds ratio for development of cardiogenic shock was 8.8 (95% CI 2.5-21).

Conclusions

Patients with acute pulmonary embolism with elevated serum cTnI levels are at a higher risk for the development of right ventricular dysfunction and cardiogenic shock. Serum cTnI has a role in risk stratification and short-term prognostication in patients with acute pulmonary embolism.     

A new thrombolytic agent,monteplase, is independent of the plasminogen activator inhibitor in patients with acute myocardial infarction: initial results of the COmbining Monteplase with Angioplasty (COMA) trial

Background Both thrombolytic therapy and coronary angioplasty have been inconsistent together for primary acute myocardial infarction (AMI) therapy, because conventional thrombolytic agents accelerate plasminogen activator inhibitor-1 (PAI-1) activity. However, combining newly developed mutant tissue-type plasminogen activators with coronary angioplasty should be reconsidered. Methods This study was designed to investigate clinical usefulness of such an agent, monteplase, for treatment of AMI in light of PAI-1 kinetics. One hundred fifty-four consecutive patients with AMI were randomly assigned to receive direct coronary angioplasty (Group I) or coronary angioplasty after pretreatment with intravenous monteplase (Group II). In 90 of these patients, total PAI-1 antigen levels were serially measured. Results Baseline PAI-1 levels at admission were higher in patients with occluded infarct-related arteries than in patients with patent arteries in Group I (39 ± 4 vs 20 ± 2 ng/mL, P < .01) and in Group II (36 ± 3 vs 27 ± 2 ng/mL, P < .05). In the high PAI-1 level subgroup (≥27 ng/mL, n = 53), Group II showed a higher patency rate than Group I (56 vs 18%, P < .01). Multiple logistic regression analysis indicated that patency could be predicted by the PAI-1 level in Group I (Wald χ²= 3.94, P = .02, odds ratio 0.924, 95% CI 0.855-0.999), but not in Group II. Serial change patterns in the PAI-1 level were identical in Group I and Group II. Conclusion Because monteplase can be used independently of PAI-1 kinetics, a combination of monteplase administration at a community hospital with prompt transfer to a tertiary center for coronary intervention may be a powerful strategy for AMI. (Am Heart J 2002;144:e5.)     

Effect of plaque debulking before stent implantation on in-stent neointimal proliferation: a serial 3-dimensional intravascular ultrasound study

Background

Recent intravascular ultrasound (IVUS) studies have suggested that plaque burden has a role in promoting intimal hyperplasia after stenting. We report on volumetric assessments of in-stent neointimal formation with 3-dimensional IVUS analysis, comparing directional coronary atherectomy (DCA) plus stenting (DCA/stenting) to stenting without DCA.

Methods

Twenty-four patients (24 lesions) treated with DCA before stenting were matched to 24 patients (24 lesions) receiving stenting without DCA. All stents were a single Multilink stent. In both groups, serial IVUS was performed before and after intervention and during the 6-month follow-up period. The arterial segments that were analyzed with a computer-based contour detection program were the same as the stented segments analyzed on serial studies. These measurements were obtained: (1) lumen volume (LV), (2) stent volume (SV), (3) vessel volume (VV), (4) in-stent neointimal volume (ISV) calculated as SV-LV, and (5) percent in-stent neointimal volume (%ISV) calculated as ([SV-LV]/SV) × 100.

Results

Baseline characteristics of the 2 groups were similar. After intervention, both groups achieved similar LV (140.0 mm³ DCA/stenting vs 135.2 mm³ stenting alone). However, the follow-up ISV and %ISV were significantly smaller in the DCA/stenting group (19.6 ± 12.2 mm³ DCA/stenting vs 44.6 ± 29.5 mm³ stenting alone; P = .00040; 15.3% ± 10.6% DCA/stenting vs 31.5% ± 17.7% stenting alone; P = .00040). Consequently, the DCA/stenting group showed a significantly greater follow-up LV (121.0 ± 51.5 mm³ DCA/stenting vs 91.5 ± 26.7 mm³ stenting alone; P = .016).

Conclusions

Plaque removal with DCA before stenting inhibits in-stent neointimal hyperplasia.     

Randomized comparison of debulking followed by stenting versus stenting alone for ostial left anterior descending artery stenosis: intravascular ultrasound guidance

Background

Although directional coronary atherectomy (DCA) before stenting has the advantage of combining substantial removal of atheromatous plaque and prevention of elastic recoil, there has been no randomized study to investigate its efficacy in ostial left anterior descending artery (LAD) lesions. This study was aimed to evaluate the effect of DCA followed by stenting on ostial LAD stenosis under the guidance of intravascular ultrasound (IVUS).

Methods

Eighty-six patients with ostial LAD stenoses were randomly assigned to DCA followed by stenting (group I) or stenting alone (group II). Aggressive DCA or optimal stenting was performed in both groups under the guidance of IVUS. The primary end point was angiographic restenosis at 6 months.

Results

Baseline clinical and angiographic characteristics were similar between the 2 groups. The postprocedural minimal lumen diameter was larger in group I than group II (4.0 ± 0.4 mm vs. 3.5 ± 0.5 mm, P < .001). However, the angiographic restenosis rates were not significantly different between the 2 groups (9/32 [28.1%] in group I vs. 11/30 [36.7%] in group II, P = .472). The postprocedural IVUS stent area was the only independent determinant of restenosis by multivariate analysis (odds ratio .61, 95% CI 0.41-0.92, P = .018).

Conclusions

DCA followed by stenting achieved greater lumen gain than stenting alone for ostial LAD stenosis. However, DCA did not improve angiographic restenosis.     

Prognostic importance of the oxidized product of catecholamines,adrenolutin, in patients with severe heart failure

Objectives

The purpose of this study was to assess whether adrenolutin, the inert product of the highly reactive molecules aminochromes, is increased in severe chronic heart failure and whether it is associated with a poor prognosis.

Background

Experimental evidence suggests that oxidative products of catecholamines, aminochromes, are more cardiotoxic than unoxidized catecholamines and may be increased in heart failure.

Methods

Adrenolutin was measured at baseline and at 1 and 3 months in 263 patients with chronic New York Heart Association class III or IV heart failure and a left ventricular ejection fraction of 22% ± 7%. Adrenolutin levels were compared with normal levels, and their relation to prognosis was evaluated.

Results

Baseline adrenolutin was increased (55 ± 90 pg/mL vs 8.4 ± 9.1 pg/mL for control, P < .02) and remained increased at 1 month (49 ± 65 pg/mL). During a mean follow-up of 309 ± 148 days (22-609 days), 57 patients died. Baseline adrenolutin levels correlated with mortality rates by univariate and multivariate analyses (relative risk 1.06, 95% CI 1.01-1.10 for each 17.9-pg/mL rise, P = .032). Left ventricular ejection fraction (P = .013) and New York Heart Association class (P = .009) were the only other variables associated with survival. Age, sex, plasma creatinine, plasma N-terminal atrial natriuretic peptide, and plasma norepinephrine levels were not retained in our model. Adrenolutin levels 1 month after random assignment were not significantly correlated with total mortality rate (P = .061) but were correlated with mortality rate from low output (relative risk 1.14, 95% CI 1.06-1.22, P = .002).

Conclusions

Plasma adrenolutin is increased in patients with heart failure and correlates with a poor prognosis independent of other important predictors of survival. This finding has potentially important pathophysiologic, prognostic, and therapeutic implications.     

Implications of elevated cardiac troponin T in ambulatory patients with heart failure: a prospective analysis

Background

Elevated concentrations of cardiac troponin T (TnT) have been reported in patients hospitalized for decompensated heart failure (HF). We assessed whether elevated TnT levels are associated with the severity, etiology, and prognosis of HF in stable, ambulatory patients.

Methods

From 1998-1999, we prospectively collected data from 136 ambulatory patients with HF, New York Heart Association functional class II to IV, ejection fraction ≤35%, and no recent unstable angina, myocardial infarction, surgery, or coronary revascularization. Blood was obtained and analyzed by immunoassay for TnT, and patients were followed for 14.0 ± 4.3 months for death or HF hospitalization (primary end point) and other adverse cardiovascular outcomes.

Results

Thirty-three patients (24%) had an elevated TnT level (≥0.02 ng/mL). Mean TnT concentration did not differ by etiology of HF (0.002 ± 0.03 ng/mL vs 0.02 ± 0.04 ng/mL for ischemic and nonischemic etiologies, P = .25). Compared with patients with normal (undetectable) levels of TnT, patients with elevated TnT were significantly older, had worse functional class, and had poorer renal function. Elevated TnT concentrations were associated with increased relative risks (RR) of death or HF hospitalization (RR 2.7, 95% CI 1.7-4.3, P = .001) and death alone (RR 4.2, 95% CI 1.8-9.5, P = .001) during follow-up. Elevated TnT and New York Heart Association class were significant, independent predictors of death or HF hospitalization. Increased age and serum creatinine concentrations were significant independent predictors of death alone.

Conclusions

Nearly one fourth of ambulatory patients with chronic HF have ongoing myocardial necrosis as shown by abnormal TnT values, which are associated with increased mortality and morbidity.     

Evidence of proatherogenic inflammation in polycystic ovary syndrome

Women with polycystic ovary syndrome (PCOS) have chronic low-level inflammation that can increase the risk of atherogenesis. We measured circulating proatherogenic inflammatory mediators in women with PCOS (8 lean: body mass index, 18-25 kg/m²; 8 obese: body mass index, 30-40 kg/m²) and weight-matched controls (8 lean, 8 obese). Blood samples were obtained fasting and 2 hours after glucose ingestion to measure interleukin-6 (IL-6), soluble intercellular adhesion molecule-1 (sICAM-1), monocyte chemotactic protein-1 (MCP-1), C-reactive protein (CRP), matrix metalloproteinase-2, plasminogen activator inhibitor-1 (PAI-1), and activated nuclear factor κB in mononuclear cells. Truncal fat was determined by dual-energy x-ray absorptiometry. Fasting MCP-1 levels were elevated in lean women with PCOS compared with lean controls (159.9 ± 14.1 vs 121.2 ± 5.4 pg/mL, P < .02). Hyperglycemia failed to suppress matrix metalloproteinase-2 in lean women with PCOS compared with lean controls (1.7 ± 1.2 vs −4.8 ± 1.6 pg/mL, P < .002). Among women with PCOS, obese individuals exhibited higher fasting sICAM-1 (16.1 ± 0.8 vs 10.5 ± 1.0 ng/mL, P < .03) and PAI-1 (6.1 ± 0.7 vs 3.4 ± 0.8 ng/mL, P < .03) levels. Trend analysis revealed higher (P < .005) IL-6, sICAM-1, CRP, PAI-1, systolic and diastolic blood pressures, triglycerides, fasting insulin, and homeostasis model assessment of insulin resistance index in women with PCOS compared with weight-matched controls, and the highest levels in the obese regardless of PCOS status. Fasting MCP-1 levels correlated with activated nuclear factor κB during hyperglycemia (P < .05) and androstenedione (P < .004). Truncal fat correlated with fasting IL-6 (P < .004), sICAM-1 (P < .006), CRP (P < .0009), and PAI-1 (P < .02). We conclude that both PCOS and obesity contribute to a proatherogenic state; but in women with PCOS, abdominal adiposity and hyperandrogenism may exacerbate the risk of atherosclerosis.     

Angiographically silent left main disease detected by intravascular ultrasound: a marker for future adverse cardiac events

Background

Concomitant moderate obstructive left main (LM) disease is associated with future cardiac events and poor prognosis in patients undergoing percutaneous intervention (PCI). Whether prognosis is similarly effected by LM disease not detected by angiography, but evident on intravascular ultrasound (IVUS) imaging, is not known. The purpose of this study was to evaluate the long-term prognosis of patients with angiographically insignificant LM coronary artery disease undergoing PCI.

Methods and results

One hundred and seven consecutive patients undergoing PCI with angiographically normal or mild LM disease had 2- and 3-dimensional IVUS imaging. IVUS images were digitized, and 3-dimensional reconstruction was performed. Percent diameter and area stenosis by angiography were 4.8% ± 3.5% and 18.2% ± 9.8%, respectively. IVUS mean luminal area and area stenosis were 17.9 ± 5.6 mm² and 30.2% ± 14.7%, respectively. Long-term follow-up was available in 102 (95%) patients at a median of 29 (range 8-52) months. Major adverse cardiac events, defined as death (6), myocardial infarction (4), repeat PCI (13), or CABG (16), were associated with female sex (P = .04), diabetes (P = .02), angiographic minimum lumen diameter (P = .04), and IVUS minimum (P = .01) and mean (P = .01) lumen area. Multivariate predictors of late cardiac events were diabetes (hazard ratio 2.69, P = .014) and minimum lumen area by IVUS (hazard ratio 0.59, P = .015).

Conclusions

Despite being angiographically silent, LM disease detected by IVUS is an independent predictor of cardiac events and may serve as a marker for such events. These data extend the spectrum of LM disease severity and its relationship to cardiac prognosis in patients undergoing PCI.     

Response of B-type natriuretic peptide to exercise in hypertensive patients with suspected diastolic heart failure: correlation with cardiac function, hemodynamics, and workload

Background

Diastolic heart failure (DHF) is characterized by dyspnea due to increased left ventricular (LV) filling pressures during stress. We sought the relationship of exercise-induced increases in B-type natriuretic peptide (BNP) to LV filling pressures and parameters of cardiovascular performance in suspected DHF.

Methods

Twenty-six treated hypertensive patients with suspected DHF (exertional dyspnea, LV ejection fraction >50%, and diastolic dysfunction) underwent maximal exercise echocardiography using the Bruce protocol. BNP, transmitral Doppler, and tissue Doppler for systolic (Sa) and early (Ea) and late (Aa) diastolic mitral annular velocities were obtained at rest and peak stress. LV filling pressures were estimated with E/Ea ratios.

Results

Resting BNP correlated with resting pulse pressure (r=0.45, P=0.02). Maximal exercise performance (4.6 ± 2.5min) was limited by dyspnea. Blood pressure increased with exercise (from 143 ± 19/88 ± 8 to 191 ± 22/ 90 ± 10 mm Hg); 13 patients (50%) had a hypertensive response. Peak exercise BNP correlated with peak transmitral E velocity (r = 0.41, P < .05) and peak heart rate (r = −0.40, P < .05). BNP increased with exercise (from 48 ± 57 to 74 ± 97 pg/mL, P = .007), and the increment of BNP with exercise was associated with maximal workload and peak exercise Sa, Ea, and Aa (P < .01 for all). Filling pressures, approximated by lateral E/Ea ratio, increased with exercise (7.7 ± 2.0 to 10.0 ± 4.8, P < .01). BNP was higher in patients with possibly elevated filling pressures at peak exercise (E/Ea >10) compared to those with normal pressures (123 ± 124 vs 45 ± 71 pg/mL, P = .027).

Conclusions

Augmentation of BNP with exercise in hypertensive patients with suspected DHF is associated with better exercise capacity, LV systolic and diastolic function, and left atrial function. Peak exercise BNP levels may identify exercise-induced elevation of filling pressures in DHF.     

Active Lipid Management In Coronary Artery Disease (ALMICAD) study

Purpose

Many providers have implemented specialized lipid clinics to more effectively identify, monitor, and treat hyperlipidemia in patients with coronary artery disease. The effectiveness of such a strategy is not known. We sought to investigate whether a specialized clinic achieves better lipid results and clinical outcomes than standard care.

Subjects and Methods

A total of 1233 patients who had coronary disease documented by coronary angiography were randomized to lipid clinic or standard care groups by their providers and followed for 2 years. The primary end point was a composite of death, myocardial infarction, repeat revascularization, and stroke.

Results

Lipid clinic (n = 617) and standard care (n = 616) groups had no significant baseline differences. After 2 years, the lipid clinic group had similar total cholesterol (166 ± 42 mg/dL vs 166 ± 41 mg/dL, P = .83), low-density lipoprotein cholesterol levels (84 ± 32 vs 85 ± 32, P = .28), and percentage of patients with low-density lipoprotein cholesterol less than 100 mg/dL (77.5% vs 77.6%, P = .97). There were no significant differences in the primary end point (12.3% vs 11.4%, P = .60) and mortality (7.6% vs 7.3%, P = .80) between the lipid clinic and standard care groups.

Conclusions

In patients identified by diagnostic coronary angiography and managed within a single health care system, implementation of a specialized lipid clinic did not achieve greater attainment of hyperlipidemia treatment goals or improved cardiac outcomes.     

Comprehensive analysis of intravascular ultrasound and angiographic morphology of culprit lesions between ST-segment elevation myocardial infarction and non-ST-segment elevation acute coronary syndrome

Background

Some plaques lead to ST-segment elevation myocardial infarction (STEMI), whereas others cause non-ST-segment elevation acute coronary syndrome (NSTEACS). We used angiography and intravascular ultrasound (IVUS) to investigate the difference of culprit lesion morphologies in ACS.

Methods

Consecutive 158 ACS patients whose culprit lesions were imaged by preintervention IVUS were enrolled (STEMI = 81; NSTEACS = 77). IVUS and angiographic findings of the culprit lesions, and clinical characteristics were compared between the groups.

Results

There were no significant differences in patients' characteristics except for lower rate of statin use in patients with STEMI (20% vs 44%, p = 0.001). Although angiographic complex culprit morphology (Ambrose classification) and thrombus were more common in STEMI than in NSTEACS (84% vs 62%, p = 0.002; 51% vs 5%, p < 0.0001, respectively), SYNTAX score was lower in STEMI (8.6 ± 5.4 vs 11.5 ± 7.1, p = 0.01). In patients with STEMI, culprit echogenicity was more hypoechoic (64% vs 40%, p = 0.01), and the incidence of plaque rupture, attenuation and “microcalcification” were significantly higher (56% vs 17%, p < 0.0001; 85% vs 69%, p = 0.01; 77% vs 61%, p = 0.04, respectively). Furthermore, the maximum area of ruptured cavity, echolucent zone and arc of microcalcification were significantly greater in STEMI compared with NSTEACS (1.80 ± 0.99 mm² vs 1.13 ± 0.86 mm², p = 0.006; 1.52 ± 0.74 mm² vs 1.21 ± 0.81 mm², p = 0.004; 99.9 ± 54.6° vs 77.4 ± 51.2°, p = 0.01, respectively). Quantitative IVUS analysis showed that vessel and plaque area were significantly larger at minimum lumen area site (16.6 ± 5.4 mm² vs 14.2 ± 5.5 mm², p = 0.003; 13.9 ± 5.1 mm² vs 11.6 ± 5.2 mm², p = 0.003, respectively).

Conclusion

Morphological feature (outward vessel remodeling, plaque buildup and IVUS vulnerability of culprit lesions) might relate to clinical presentation in patients with ACS.     

Short- and long-term beneficial effects of trimetazidine in patients with diabetes and ischemic cardiomyopathy

Background

Trimetazidine (TMZ) has been shown to partially inhibit free fatty acid oxidation by shifting substrate utilization from fatty acid to glucose. The aim of this study was to assess the effects of TMZ in patients with diabetes and ischemic cardiomyopathy.

Methods

Sixteen patients with diabetes and ischemic hypokinetic cardiomyopathy (all males) on conventional therapy were randomized to receive either placebo or TMZ (20 mg 3 times per day), each arm lasting 15 days, and then again to receive either placebo or TMZ for 2 additional 6-month periods, according to a double-blind, crossover design. At the end of each period, all patients underwent exercise testing, 2-dimensional echocardiography, and hyperinsulinemic/euglycemic clamp. Among the others, New York Heart Association class, ejection fraction, exercise time, fasting blood glucose, end-clamp M value (index of total body glucose disposal) and endothelin-1 levels were evaluated.

Results

Both in the short and long term (completed by 13 patients), on TMZ compared to placebo, ejection fraction (47 ± 7 vs 41 ± 9 and 45 ± 8 vs 36 ± 8%, P < .001 for both) and M value (4.0 ± 1.8 vs 3.3 ± 1.6, P = .003, and 3.5 ± 1.5 vs 2.7 ± 1.6 mg/kg body weight/min, P < .01) increased, while fasting blood glucose (121 ± 30 vs 136 ± 40, P = .02 and 125 ± 36 vs 140 ± 43, P = .19) and endothelin-1 (8.8 ± 3.8 vs 10.9 ± 3.8, P < .001 and 6.2 ± 2.4 vs 9.2 ± 4.3 pg/mL, P = .03) decreased. In the short term, 10 patients decreased 1 class on the NYHA scale during treatment with TMZ (P = .019 vs placebo). Eight patients decreased 1 NYHA class while on long-term TMZ treatment, while on placebo 1 patient increased 1 NYHA class and none improved (P = .018 vs placebo).

Conclusions

In a short series of patients with diabetes and ischemic cardiomyopathy, TMZ improved left ventricular function, symptoms, glucose metabolism, and endothelial function. Shifting energy substrate preference away from fatty acid metabolism and toward glucose metabolism by TMZ appears an effective adjunctive treatment in patients with diabetes with postischemic cardiomyopathy.     

Ultrasound study of the prevalence of plaque at the carina in lesions that affect the coronary bifurcation. Implications for treatment with provisional stent

Introduction and objectives

The plaque distribution patterns in coronary bifurcation lesions are not well understood. It has been speculated that carina is free of plaque partly because of high wall shear stress providing an atheroprotective effect. To study plaque distribution with intravascular ultrasound (IVUS) in the coronary bifurcation and the prevalence of carina involvement.

Methods

IVUS study was performed on 195 coronary bifurcation lesions in the main vessel (MV) and on 91 in the side branch (SB). Plaque at the carina was considered when its thickness was > 0.3 mm. Plaque burden was measured at different levels: proximal reference, distal, carina and at the point of minimal lumen area (MLA).

Results

The prevalence of plaque at the carina was 32%. Its thickness was 0.8 (0.36) mm, less than that observed at the counter-carina [1.22 (0.54) mm; P < .01]. The prevalence was higher (52%) when the MLA point was distal to the carina. The plaque at the carina was associated with a lower incidence of damage at the SB ostium after stenting the MV (32% vs 54%; P < .04).

Conclusions

The carina is not immune to atherosclerosis, showing plaque at this level in one third of the bifurcations. The incidence of plaque is higher in those bifurcations with the MLA point distal to the carina and seems to be associated with a lower incidence of damage to the SB ostium.Full English text available from: www.revespcardiol.org     

Evidence for association between endothelial nitric oxide synthase gene polymorphism (G894T) and inflammatory markers: the ATTICA study

Background

We evaluated the effect of the point mutation of guanine to thymine at nucleotide position 894 (G894T) of the endothelial nitric oxide synthase (eNOS) gene on inflammatory and oxidative stress markers.

Methods

We studied genetic information from 270 men (18-87 years old) and 325 women (18-89 years old). Participants without any clinical evidence of cardiovascular or other atherosclerotic disease were randomly selected from the general population according to the age-sex distribution of Athens greater area. Genomic DNA was extracted from 2 to 5 mL of fresh or frozen whole blood using standard methods.

Results

The DNA analysis showed that 10.6% of the participants were Asp-homozygotes (Asp/Asp), 40% heterozygotes (Asp/Glu) and 49.4% Glu-homozygotes (Glu/Glu). Compared to Asp/Glu and Glu/Glu, Asp/Asp had higher levels of fibrinogen (332 ± 46 or 329 ± 33 vs 319 ± 29 mg/dL, P = .029), white blood cells (6.9 ± 0.6 or 6.5 ± 0.3 vs 6.1 ± 0.9 × 10³ counts, P = .044), and oxidized low-density lipoprotein cholesterol (68 ± 21 or 61 ± 22 vs 59 ± 20 mg/dL, P = .039), after controlling for several potential confounders. An insignificant association was found between homocysteine (P = .08), C-reactive protein (P = .096), and the distribution of G894T polymorphism (P < .1). No association between the distribution of the polymorphism and hypertension status of the participants was observed.

Conclusions

Our results imply that G894T polymorphism of the endothelial nitric oxide synthase gene is associated with elevated levels of inflammatory and oxidative stress markers, which may partially explain the increased prevalence of G894T polymorphism among patients with cardiovascular disease.     

Multislice Computed Tomographic Coronary Angiography for Quantitative Assessment of Culprit Lesions in Acute Coronary Syndromes

Background

We studied the characteristics of low-density plaque (LDP) burden in patients with acute coronary syndrome (ACS), using 64-slice computed tomography (CT) assessment. Though several CT plaque features such as positive remodelling, adjacent spotty calcification or the presence of LDP have been demonstrated to be associated with unstable plaques, it is still unknown whether their severity and extent present any differences between different types of ACS.

Methods

In 45 subjects with ACS (22 unstable angina and 23 non–ST-elevation myocardial infarction [NSTEMI]), 118 coronary plaques were evaluated using a CT multislice 64 assessment including the burden with atheroma having a CT density below 30, 60, or 100 Hounsfield units (HU), remodelling index and spotty calcification.

Results

Culprit lesions tend to be larger in volume (111.11 mm³ vs 62.25 mm³; P < 0.0001), have a higher remodelling index (1.27 vs 1.01; P < 0.0001), and present a significantly larger LDP with a density < 30 HU (23.3 mm³ vs 7.6 mm³; P < 0.0001) or < 60 HU (33.4 mm³ vs 16.9 mm³; P < 0.0001) than nonculprit lesions. The presence of a plaque more than 20 mm³ in volume with a CT density < 30 HU (P = 0.0009) and the presence of all 3 markers of plaque vulnerability (LDP, spotty calcifications or positive remodelling) (P = 0.01) significantly correlated with the presence of an NSTEMI.

Conclusions

Culprit lesions demonstrated larger plaque volumes, a higher burden with low-density cores, and more intense remodelling than nonculprit lesions, whereas culprit lesions associated with NSTEMI showed a higher burden with lower density cores than those associated with unstable angina.