Effect of Optimal Medical Therapy Before Procedures on Outcomes in Coronary Patients Treated With Drug-Eluting Stents.

It has not been established whether the achievement of optimal medical therapy (OMT) before implantation of a drug-eluting stent has a clinical benefit for patients with stable coronary artery disease (CAD). This study included 3,004 patients with CAD treated with drug-eluting stent from 123 Japanese participating centers. The achievement of OMT was defined as control of blood pressure <130/80 mm Hg, hemoglobin A1c <7.0%, and low-density lipoprotein cholesterol <100 mg/dl. The primary end point was target vessel failure, a composite of death related to the target vessel, myocardial infarction, or clinically driven revascularization at 24 months after stent implantation. Immediately before the procedure, only 548 patients (18.2%) had achieved all 3 target criteria (the achieved OMT group), whereas the remaining 2,456 patients failed to achieve one or more criteria (the non-OMT group). At 24 months, the incidence of target vessel failure was 7.0% in the achieved OMT group versus 10.0% in the non-OMT group (hazard ratio 0.68, 95% CI 0.48 to 0.96, p = 0.03). The incidence of non-Q-wave myocardial infarction was also lower in the achieved OMT group than in the non-OMT group (0.5% vs 1.5%, p = 0.08). Multivariate logistic regression analysis identified that hemoglobin A1c <7.0% was the only protective predictor of 24-month target vessel failure (odds ratio 0.56, 95% CI 0.43 to 0.73, p <0.01). In conclusion, this study demonstrated that in patients with stable CAD scheduled for stent implantation, achievement of OMT before percutaneous coronary intervention significantly reduced subsequent cardiac events. Achievement of OMT is still insufficient in modern clinical practice.

Three-year follow-up outcomes of SES and PES in a randomized controlled study stratified by the presence of diabetes mellitus: J-DEsSERT trial.

BACKGROUND: Three-year clinical follow-up of patients with diabetes mellitus (DM) in the Japan-Drug Eluting Stents Evaluation; a Randomized Trial (J-DESsERT) using 2 different drug eluting stents (DES). A recent study demonstrated that efficacy of sirolimus eluting stents (SES) attenuated over time in diabetic patients. METHODS: In the largest trial of its kind, 1724 DM patients out of 3533 enrolled patients were randomized to either SES or paclitaxel eluting stents (PES). RESULTS: There were no significant differences in baseline clinical characteristics aside from hypertension. Incidence of major adverse cardiac cerebrovascular events (MACCE) mainly due to higher target vessel failure (TVF) initially indicated a benefit in SES (MACCE rate at 1 year: SES 9.4%, PES 12.2%, p=0.08); however this had attenuated by the time of the 3-year follow-up (MACCE rate from 1 to 3 years: SES 8.4%, PES 6.1%, p=0.10). A similar pattern was observed in insulin-treated patients: MACCE rate from 1 to 3 years was 10.5% in SES and 6.4% in PES (p=0.25). Angiographic follow-up also resulted in higher major adverse cardiac event (MACE) rates at 1 year (presence 11.5%, absence 8.3%, p=0.04); however by 3 years rates were similar regardless of the presence of angiographic follow-up (MACE rate at 3 years: presence 16.0%, absence 14.5%, p=0.35). CONCLUSIONS: The superiority of SES over PES in MACCE at 1 year had attenuated by 3-year follow-up. Eventually, the 3-year safety and efficacy profiles were similar regardless of insulin treatment.

Presence of myocardial hypoenhancement on multidetector computed tomography after primary percutaneous coronary intervention in acute myocardial infarction predicts poor prognosis.

BACKGROUND: Recent research has suggested that patients with greater delayed contrast-enhanced size by multidetector computed tomography (MDCT) are more likely to experience adverse cardiac events and have poor prognoses over the long term. The myocardial hypoenhancement area in the delayed contrast-enhanced effect suggests microvascular obstruction. The outcomes of patients with a hypoenhancement area detected by MDCT have not been clear. We examined the clinical importance of myocardial hypoenhancement detected by delayed contrast-enhanced MDCT after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction. METHODS AND RESULTS: In 80 patients with acute myocardial infarction, MDCT was performed immediately after primary PCI. We investigated the outcomes of the patients with hypoenhancement detected by MDCT. Myocardial hypoenhancement was observed in 14 patients (17.5%). All 14 of these patients with hypoenhancement had a transmural infarction, and their infarct volume was significantly higher than those of the patients without hypoenhancement (n=66). During the median follow-up period of 309 days, the appearance of myocardial hypoenhancement was associated with the presence of slow flow/no-reflow, time from onset to reperfusion ≥6 h, aging, smoking, chronic kidney disease, and hyper-low-density lipoprotein cholesterolemia. The incidence of major adverse cardiovascular events (MACE) was significantly higher in the patients with hypoenhancement compared to those without hypoenhancement, regardless of the myocardial infarct volume. CONCLUSIONS: These results indicate that the presence of myocardial hypoenhancement in delayed contrast-enhanced MDCT after PCI as well as the extent of infarct area is an important predictor of MACE.

Outcomes of the largest multi-center trial stratified by the presence of diabetes mellitus comparing sirolimus-eluting stents (SES) and paclitaxel-eluting stents (PES) in patients with coronary artery disease. The Japan drug-eluting stents evaluation: a randomized trial (J-DESsERT).

The Japan drug-eluting stents evaluation: a randomized trial (J-DESsERT) was conducted to compare the effectiveness of 2 different drug-eluting stents (DES). It remains uncertain which is more efficacious in diabetic patients, sirolimus-eluting stents (SES) or paclitaxel-eluting stents (PES). In this trial, the largest of its kind, 3,533 patients including 1,724 diabetes mellitus (DM) patients were randomized to either SES or PES. Stratification was based on the presence or absence of DM. PES target vessel failure (TVF) non-inferiority at 8 months (primary endpoint) was not demonstrated when compared to SES (SES 4.5 % vs. PES 6.4 %, p = 0.23). In addition, PES TVF superiority at 8 months in the DM subset (secondary endpoint) was not shown (SES 5.6 % vs. PES 7.6 %, p = 0.10). Insulin treatment was associated with increased TVF rates, however, this was less pronounced in the PES group. At 8 months, the similar TVF rates for SES and PES up to that point diverged significantly, favoring SES out to 12 months. Patients undergoing routine angiographic follow-up demonstrated lower TVF prior to the 8-month point, and higher TVF after 8 months, as compared to those followed clinically. In conclusion, the current study failed to demonstrate the proposed superiority of PES for DM patients. In addition, the diversion of TVF at 8 months may reflect an "oculo-stenotic reflex" bias (the tendency to treat lesions found during routine, rather than clinically driven, angiographic follow-up), which could constitute an obstacle for evaluating the true clinical effect of new devices.

Impact of angiographic peri-stent contrast staining (PSS) on late adverse events after sirolimus-eluting stent implantation: an observation from the multicenter j-Cypher registry PSS substudy.

This study sought to assess clinical significance of angiographic peri-stent contrast staining (PSS) after sirolimus-eluting stent (SES) implantation in a large multicenter study with 5-year follow-up. The j-Cypher PSS substudy is a multicenter study including 5712 patients (7838 lesions) who underwent follow-up angiographic study within 12 months after SES implantation. Late acquired PSS was observed in 184 patients (3.2 %) or 194 lesions (2.5 %). Independent risk factors of PSS were chronic total occlusion and left anterior descending artery lesion, while negative risk factors were in-stent restenosis, diabetes mellitus, ≥70 years of age, and left circumflex coronary artery lesion. Cumulative incidence of definite very late stent thrombosis (VLST) at 4 years after the index follow-up angiography in lesions with PSS was significantly higher than that in lesions without PSS (5.3 versus 0.7 %, P < 0.0001). Late target-lesion revascularization (TLR) was also more frequently observed in the PSS group (13 versus 6.9 %, P = 0.01), while late TLR for restenosis excluding those TLR procedures for VLST tended to be higher in the PSS group (9.9 versus 6.3 %; P = 0.15). PSS found in 2.5 % of lesions within 12 months after SES implantation was associated with higher risk for subsequent VLST.

Rescue pulmonary vein isolation for hemodynamically unstable atrial fibrillation storm in a patient with an acute extensive myocardial infarction.

BACKGROUND: New-onset atrial fibrillation in patients hospitalized for an acute myocardial infarction often leads to hemodynamic deterioration and has serious adverse prognostic implications; mortality is particularly high in patients with congestive heart failure and/or a reduced left ventricular ejection fraction. The mechanism of atrial fibrillation in the context of an acute myocardial infarction has not been well characterized and an effective treatment other than optimal medical therapy and mechanical hemodynamic support are expected. CASE PRESENTATION: A 71 year-old male with an acute myocardial infarction due to an occlusion of the left main coronary artery was treated with percutaneous coronary intervention. He had developed severe congestive heart failure with a left ventricular ejection fraction of 34%. The systemic circulation was maintained with an intraaortic balloon pump, continuous hemodiafiltration, and mechanical ventilation until atrial fibrillation occurred on day 3 which immediately led to cardiogenic shock. Because atrial fibrillation was refractory to intravenous amiodarone, beta-blockers, and a total of 15 electrical cardioversions, the patient underwent emergent radiofrequency catheter ablation on day 4. Soon after electrical cardioversion, ectopies from the right superior pulmonary vein triggered the initiation of atrial fibrillation. The right pulmonary veins were isolated during atrial fibrillation. Again, atrial fibrillation was electrically cardioverted, then, sinus rhythm was restored. Subsequently, the left pulmonary veins were isolated. The stabilization of the hemodynamics was successfully achieved with an increase in the blood pressure and urine volume. Hemodiafiltration and amiodarone were discontinued. The patient had been free from atrial fibrillation recurrence until he suddenly died due to ventricular fibrillation on day 9. CONCLUSIONS: To the best of our knowledge, this is the first report of pulmonary vein isolation for a rescue purpose applied in a patient with hemodymically unstable atrial fibrillation complicated with an acute myocardial infarction. This case demonstrates that ectopic activity in the pulmonary veins may be responsible for triggering atrial fibrillation in the critical setting of an acute myocardial infarction and thus pulmonary vein isolation could be an effective therapeutic option.

A case of fulminant myocarditis associated with novel N1H1 influenza successfully treated by percutaneous cardiopulmonary support system.

We report a case of fulminant myocarditis associated with N1H1 influenza virus infection. N1H1 was confirmed by a polymerase chain reaction assay and she was treated with oseltamivir phosphate. She was admitted to the hospital because of respiratory distress, however, echocardiography revealed severely depressed wall motion followed by refractory ventricular fibrillation. Extracorporeal circulation by emergent percutaneous cardiopulmonary support system was required to maintain hemodynamic stability. Cardiac function was spontaneously and gradually restored within a week. Findings from biopsy samples taken on day 1 and day 23 were consistent with acute myocarditis.

Renal protective effects and the prevention of contrast-induced nephropathy by atrial natriuretic peptide.

OBJECTIVES: This study was designed to examine the protective effects of atrial natriuretic peptide (ANP) on contrast-induced nephropathy (CIN) after coronary angiography. BACKGROUND: Contrast-induced nephropathy is a common complication after angiography. Some studies have shown that ANP has renal protective effects, but the beneficial effects for CIN prevention remain to be clearly shown. METHODS: In a prospective, controlled, randomized trial in 254 consecutive patients with serum creatinine concentrations of > or =1.3 mg/dl, patients received either ANP (0.042 microg/kg/min; ANP group, n = 126) or Ringer solution alone (control group, n = 128). Treatment of either type was initiated 4 to 6 h before angiography and continued for 48 h. RESULTS: There were no significant differences in age, sex, diabetes mellitus, or baseline serum creatinine level between the 2 groups. The prevalence of CIN, defined as a 25% increase in creatinine or an increase in creatinine of > or =0.5 mg/dl from baseline within 48 h, was significantly lower in the ANP group than in the control group (3.2% vs. 11.7%, respectively; p = 0.015). Multivariate analysis revealed that the use of >155 ml of contrast medium (odds ratio: 6.89; p < 0.001) and ANP treatment (odds ratio: 0.24; p = 0.016) were significant predictors of developing CIN. The incidence of an increase in creatinine of > or =25% or of > or =0.5 mg/dl from baseline at 1 month was also significantly lower in the ANP group than in the control group (p = 0.006). CONCLUSIONS: In addition to hydration, ANP administration is effective in the prevention of CIN in patients with chronic renal failure, and the effect was maintained for 1 month.

Demonstration of left ventricular dyssynchrony and resynchrony by ECG-gated SPECT with cardioGRAF in a patient with advanced heart failure and narrow QRS complex.

Accurate objective quantification of left ventricular (LV) dyssynchrony is a key to selecting candidates for cardiac resynchronization therapy (CRT), especially when screening among patients with a narrow QRS. CardioGRAF (cardio Gated single photon emission computed tomography Regional Assessment for left ventricular Function), a newly developed LV segmental time-volume analyzing program for myocardial perfusion single photon emission tomography, may be a promising tool. We describe the case of a 63-year-old male with non-ischemic cardiomyopathy with a QRS duration of 112 ms, in whom cardioGRAF successfully demonstrated baseline LV dyssynchrony and resynchronization achieved by CRT as evidenced by a significant decrease in dyssynchrony index (standard deviation of the duration from R to end-systole among 17 LV segments) x100/R-R interval).

Risk stratification of patients with prior myocardial infarction and advanced left ventricular dysfunction by gated myocardial perfusion SPECT imaging.

BACKGROUND: The Multicenter Automatic Defibrillator Implantation Trial II (MADIT-II) has shown that the prophylactic implantable cardiac defibrillator improves the survival rate of patients with prior myocardial infarction and advanced left ventricular (LV) dysfunction. However, a more accurate noninvasive predictor should be found to identify subgroups at high risk, one that would allow implantable cardiac defibrillator therapy to be directed specifically to the patients who would benefit most. METHODS AND RESULTS: To elucidate whether technetium 99m tetrofosmin electrocardiogram-gated single photon emission computed tomography (SPECT) imaging at rest can determine the risk of arrhythmic death, 106 patients who met the MADIT-II criteria (LV ejection fraction 1 month earlier, and no sustained ventricular tachyarrhythmia) were recruited from a pool of 4628 consecutive patients who had undergone resting Tc-99m tetrofosmin SPECT imaging. By use of the endpoints of lethal arrhythmic events, which included documentation of sustained ventricular tachycardia, ventricular fibrillation, or diagnosis of sudden cardiac death, we performed follow-up for a mean of 30 months. Lethal arrhythmic events occurred in 14 patients. Patients with lethal arrhythmic events had a lower LV ejection fraction, greater LV end-systolic and end-diastolic volume indices, and a greater perfusion defect volume than the remaining patients. By receiver operating characteristic curve analysis, myocardial defect volume was the strongest predictor for the development of lethal arrhythmic events. CONCLUSION: Our results confirm that perfusion defect volume by Tc-99m tetrofosmin scintigraphy is the most pivotal predictor of the future occurrence of lethal arrhythmic events and of sudden cardiac death. Tc-99m tetrofosmin SPECT images may assist in identifying subsets of patients with a greater likelihood of arrhythmic death among patients with LV dysfunction.

Acute myocardial infarction caused by spontaneous postpartum coronary artery dissection.

BACKGROUND: A 34-year-old postpartum woman presented at hospital with chest pain. She had experienced an uneventful delivery of a healthy infant and had no known coronary risk factors. Electrocardiography demonstrated an acute myocardial infarction, which resolved on intravenous glyceryl trinitrate infusion. Coronary angiography revealed diffuse narrowing of the left anterior descending artery and tapering of the left main trunk, but there were no obvious hallmarks of intimal dissection. INVESTIGATIONS: Electrocardiography, coronary angiography, multidetector CT and intravascular ultrasonography. DIAGNOSIS: Postpartum coronary artery dissection. MANAGEMENT: The lesion was stabilized with orally administered amlodipine, aspirin, ticlopidine and pitavastatin, along with intravenous heparin and glyceryl trinitrate. The patient was later discharged on bisoprolol, aspirin, pitavastatin and temocapril.

Asymptomatic Brugada syndrome associated with postural orthostatic tachycardia syndrome: Does autonomic disorder increase propensity for future arrhythmic events?

Autonomic imbalance may work as a modifying factor for initiating lethal arrhythmia in patients with Brugada syndrome. A 26-year-old man with episodes of near syncope was given a diagnosis of an autonomic disorder, postural orthostatic tachycardia syndrome (POTS). The patient spontaneously showed typical Brugada-type ECG, and ventricular fibrillation was induced by programmed electrical stimulation, which allowed the further diagnosis of Brugada syndrome. Although it seems that Brugada syndrome is asymptomatic, its uncommon association of POTS may increase the risk for future arrhythmic events in this patient.

Effects of low-dose angiotensin II receptor blocker candesartan on cardiovascular events in patients with coronary artery disease.

OBJECTIVES: The purpose of this study was to investigate the effects of angiotensin II receptor blockers on the prevention of cardiovascular events in patients with coronary artery disease (CAD). BACKGROUND: Angiotensin II may contribute to the pathogenesis of CAD. Long-term clinical trials have shown that blockade of the renin-angiotensin system can reduce cardiovascular events in patients with acute myocardial infarction complicated by heart failure. METHODS: Patients with a history of coronary intervention and no significant coronary stenosis on follow-up angiography 6 months after intervention were randomly assigned into a candesartan group (n = 203; baseline treatment plus candesartan 4 mg/d) or a control group (n = 203; baseline treatment alone). The primary end point was a composite of revascularization, nonfatal myocardial infarction, or cardiovascular death. The secondary end point was hospitalization for cardiovascular causes. RESULTS: There were no changes in blood pressure and in other coronary risk factors in either group during a mean follow-up of 24 months. Primary end point risk was significantly lower in the candesartan group (n = 12) than in control group patients (n = 25) (P =.03). Candesartan treatment reduced primary end point risk (5.9% vs 12.3% for control subjects; relative risk, 0.47; 95% CI, 0.24 to 0.93). The incidence of all events including secondary end points and noncardiovascular death was significantly lower in the candesartan group than in control group patients (23 vs 40 cases) (P =.02). CONCLUSIONS: Relatively low-dose candesartan, which did not alter blood pressure levels, reduces cardiovascular risk in high-risk patients with CAD.

Follow-up X rays play a key role in detecting implantable cardioverter defibrillator lead fracture: a case of incessant inappropriate shocks due to lead fracture.

A patient with an implantable cardioverter defibrillator (ICD) received incessant inappropriate shocks due to a lead fracture 3 years after implantation. Routine lead measurements at 3-month intervals had shown no abnormal findings even at the most recent measurement performed 2 months prior to the event. In contrast, serial observation of chest X rays clearly disclosed progressive lead narrowing starting 11 months prior to the event. This case indicates the importance of the routine chest X rays in long-term follow-up of ICDs and sets a precedent for interpreting lead narrowing in such X rays.

Angiotensin II type 2 receptor blockade partially negates antihypertrophic effects of type 1 receptor blockade on pressure-overload rat cardiac hypertrophy.

We investigated the effects of angiotensin II type 2 (AT2) receptor blockade on the antihypertrophic effects of type 1 receptor (AT1) blockade in pressure-overload cardiac hypertrophy in adult rats. Cardiac hypertrophy was induced by banding the abdominal aorta above the renal arteries. The rats were treated with either an AT1 receptor antagonist TCV-116 (TCV, 10 mg/kg/day), an AT2 receptor antagonist PD123319 (PD, 20 mg/kg/day), or both for 4 weeks after the aortic banding. We measured systolic and diastolic blood pressure (BP), body weight (BW), left ventricular weight (LVW), and serum and cardiac angiotensin converting enzyme (ACE) activities. Aortic banding increased BP and LVW/BW, and TCV reversed both these increases. PD affected neither BP nor LVW/BW. TCV+PD reversed the increase in BP but not LVW/BW. Thus, PD was considered to counteract the antihypertrophic effect of TCV without affecting BP. All three treatments reduced cardiac ACE activity without affecting serum ACE activity. Our data demonstrated that AT2 receptor blockade negates the antihypertrophic effects of AT1 receptor blockade in an adult rat model of pressure-overload cardiac hypertrophy. AT2 receptors may mediate the signaling pathways involved in growth inhibition, which could counteract mediation of the cellular growth signaling pathways by AT1 receptors.

The Glu298Asp polymorphism in endothelial nitric oxide synthase gene is associated with coronary in-stent restenosis.

BACKGROUND: Reduced or impaired synthesis of nitric oxide promotes the proliferation of vascular smooth muscle cells, and thus may induce the neointimal formation leading to coronary in-stent restenosis. Recent reports have suggested that the Glu298Asp polymorphism in exon 7 of the endothelial nitric oxide synthase gene is associated with coronary spasm and acute myocardial infarction. In this study, we have examined the implication of this polymorphism with regard to coronary restenosis after Palmaz-Schatz stent deployment. METHODS: Eighty-nine lesions in 85 consecutive patients were treated with Palmaz-Schatz stents, and were prospectively followed up for 6 months. The lesions were classified into a restenosis group (% diameter stenosis=50%) and a non-restenosis group. Assessment was made using an automated quantitative angiographic system. We performed polymerase chain reaction-restriction fragment length polymorphism analysis to detect the missense Glu298Asp variant in exon 7 of the endothelial nitric oxide synthase gene. RESULTS: Coronary risk factors and angiographic findings of stenotic lesions did not differ between the groups. Univariate analyses showed that the missense Glu298Asp variant was the only statistically significant predictor of restenosis (odds ratio, 4.27; P=0.025). In addition, multiple logistic regression analysis revealed the missense Glu298Asp variant as the only independent predictor for in-stent restenosis (odds ratio, 3.90; P=0.036). CONCLUSIONS: The missense Glu298Asp variant may be an independent risk factor for in-stent restenosis.

Quinapril prevents restenosis after coronary stenting in patients with angiotensin-converting enzyme D allele.

Restenosis after coronary artery stent implantation is attributed chiefly to intimal hyperplasia, which is prevented experimentally by angiotensin-converting enzyme (ACE) inhibitors. Therefore, the present study investigated whether the effect of quinapril, a tissue-specific ACE inhibitor, on the prevention of coronary restenosis differs according to ACE polymorphism. One hundred consecutive patients with successful stent implantation were randomly assigned to quinapril and control groups. Both follow-up angiography and ACE polymorphism analysis were obtained from 92 patients (control, 46; quinapril treatment, 46). The prevalence of risk factors did not differ statistically according to quinapril treatment or ACE genotypes. There was no statistically significant difference in the occurrence of restenosis 6 months after stenting between the groups. Quantitative coronary angiography revealed that quinapril treatment resulted in significantly higher minimal lumen diameter and significantly lower percent diameter stenosis (22.9 +/- 22.6 vs 37.1 +/- 19.7% in the control group, p < 0.05) in patients with the D allele although there was no difference in those with the II genotype. In addition, intravascular ultrasound revealed that quinapril treatment significantly prevented the loss of minimal lumen cross-sectional area and the increase in percent area stenosis (34.5 +/- 14.0 vs 53.3 +/- 16.4% in the control group, p < 0.05) in patients with the D allele compared to those with the II genotype. These results suggest that the administration of ACE inhibitors for the attenuation of lumen loss after coronary stent implantation is best for subjects with the D allele of the ACE genotype.

Plasma C-reactive protein predicts left ventricular remodeling and function after a first acute anterior wall myocardial infarction treated with coronary angioplasty: comparison with brain natriuretic peptide.

BACKGROUND: C-reactive protein (CRP) directly participates in the myocardial injury of acute myocardial infarction (MI). Although high plasma CRP levels in the acute phase strongly indicate a poor early clinical outcome of patients with MI, the impact of CRP levels on late left ventricular (LV) function and remodeling, which are closely associated with long-term prognosis, remains unknown. HYPOTHESIS: Acute plasma CRP levels may predict late LV function and remodeling after MI. METHODS: We prospectively studied 12 consecutive patients with a first acute anterior MI recanalized by angioplasty. We measured plasma CRP levels on Days 0, 1, 2, 3, 4, and 7, and calculated the area under the curve (AUC). We also measured plasma brain natriuretic peptide (BNP) levels on Day 3 as the referential indicator of LV dysfunction and late LV remodeling. Late LV indices were independently assessed on a left ventriculogram obtained at 5.3 months to estimate the extent of LV remodeling. RESULTS: Plasma CRP reached its peak at Day 2.8 (8.68+/-4.57 mg/dl). On linear regression analysis, the AUC of CRP (35.21+/-19.33 mg/dl x day) correlated positively with BNP (316.5+/-418.6 pg/ml) (r = 0.646, p = 0.023). The AUC of CRP, peak CRP, and BNP correlated significantly with late LV indices. Among these, the AUC of CRP showed the best correlation with end-diastolic volume index (r = 0.765, p = 0.004), end-systolic volume index (r = 0.907, p < 0.001), and ejection fraction (r = -0.862, p < 0.001). CONCLUSIONS: Patients with high plasma CRP levels may be at risk for late LV dysfunction and remodeling; theoretically, their long-term prognosis may be poor. Measuring plasma CRP levels may provide valuable information for long-term risk stratification after MI.