Periodontal disease in patients with acute myocardial infarction: prevalence and contribution to elevated C-reactive protein levels

Background

Periodontal disease (PD) has been linked to adverse cardiovascular events, but the mechanism for this association is unknown. We hypothesized that PD is common in patients with acute myocardial infarction (AMI) and, when present, may result in an enhanced systemic inflammatory response with higher C-reactive protein (CRP) levels.

Methods

Periodontal examinations and serum high sensitivity CRP measurements were performed in 40 patients with AMI (11 women; mean age, 60 ± 15 years) during the index hospitalization. The control group comprised 40 sex and race frequency-matched, community volunteers (9 women; mean age, 64 ± 5 years) without known heart disease.

Results

Both the prevalence of PD and mean serum CRP levels were significantly higher in the patients with AMI than in the control subjects (48% vs 17%, P <.001 and 40.2 vs 7.9 mg/L, P <.001, respectively). Patients with AMI who had PD had significantly higher CRP levels than patients with AMI who did not have PD (50.7 vs 30.7 mg/L, P <.001). With linear regression analysis, a positive relationship was shown between the extent of PD and serum CRP levels, and with a multivariate regression model that included smoking, diabetes mellitus, infarct size and PD, PD emerged as a strong and independent predictor of elevated CRP levels (r² = 0.33, P = .004).

Conclusions

Periodontal disease is common in patients with AMI and is associated with an enhanced inflammatory response expressed by higher CRP levels. The association of PD with CRP levels in patients with AMI appears to be independent of other contributing factors.     

Pulsed wave tissue Doppler-derived myocardial performance index for the assessment of left ventricular thrombus formation risk after acute myocardial infarction

Background

Assessment of left ventricular (LV) thrombosis risk after acute myocardial infarction (AMI) is important because of potential embolic sequelae that are reduced by oral anticoagulant agents. The goal of this study was to investigate whether early assessment of LV systolic and diastolic performance with pulsed wave tissue Doppler ultrasound scanning (PWTD) predicts LV thrombosis after AMI.

Methods

Two-dimensional and Doppler ultrasound scanning echocardiographic examinations were performed in 92 consecutive patients (age, 58 ± 10 years; 11 women) with first anterior AMI within 24 hours after arrival to the coronary care unit. From the apical 4-chamber view, the mitral annular velocities were recorded at the lateral corner of the mitral annulus with PWTD. The myocardial performance index (MPI), which combines parameters of both systolic and diastolic ventricular function, was calculated from the PWTD recordings. To analyze LV thrombus formation, the 2-dimensional echocardiographic examination was repeated on days 3, 7, 15, and 30. The patients were divided in 2 groups according to LV thrombus formation.

Results

LV thrombus was found in 32 of 92 patients (35%; group 1) and was not found in 60 patients (65%; group 2). The MPI was significantly higher in group 1 than in group 2 (0.73 ± 0.20 vs 0.53 ± 0.14; P <.001). When an MPI >0.6 was used as the cutoff, LV thrombus formation could be predicted with a sensitivity rate of 81%, a specificity rate of 73%, a positive predictive value of 62%, and a negative predictive value of 88%. In multivariate analyses, only MPI and LV wall motion score index were independent predictors of LV thrombus formation (P = .038 and P = .047, respectively).

Conclusions

The MPI derived with PWTD soon after admission appears to be a useful parameter for assessing the risk of LV thrombosis after AMI. Patients with an MPI >0.6 after AMI seem to be at a higher risk for thrombus formation.     

Loratidine improves ischemic parameters of exercise stress test in patients with acute myocardial infarction

Background

This study sought to determine whether adding an anti-histaminic medication, loratidine, to anti-ischemic treatment would ameliorate or improve ischemic parameters induced by exercise stress test in patients who suffered an acute myocardial infarction.

Methods

Twenty stable patients with acute inferior myocardial infarction who had a positive EST were randomly allocated into 2 groups, A and B. Patients in group A and B received a 10 mg loratidine tablet added daily to their anti-ischemic regimen for 7 days during the second and third week post-event, respectively. At the end of each period they underwent an exercise stress test (EST). Exercise parameters in each group were then compared before and after loratidine therapy.

Results

Both groups showed improvements in exercise parameters after loratidine therapy compared to basal EST results. ST_max ( group A: 1.9 ± 0.74 vs 0.9 ± 1.29 mm, P = .046; group B: 2.5 ± 0.71 vs 1.4 ± 1.17 mm, P = .041), ST_lead ( group A: 3.4 ± 1.08 vs 1.5 ± 2.12, P = .027; group B: 4.6 ± 1.71 vs 2.22 ± 2.25, P = .011), ST_total ( group A: 4.7 ± 2.18 vs 2.1 ± 3.11 mm, P = .024; group B: 7.9 ± 2.92 vs 3.33 ± 3.81 mm, P = .005).

Conclusion

Our study revealed that loratidine, a histamine-1 receptor blocker, improves ischemic parameters of EST when given as additive therapy to a routine anti-ischemic regimen during the sub-acute phase of myocardial infarction.     

Prognostic value of admission glucose in non-diabetic patients with myocardial infarction

Background

Patients with acute myocardial infarction (AMI) who have diabetes have an increased risk of death. In nondiabetic patients, admission glucose levels may be a predictor of survival. However, data regarding admission glucose and long-term outcome in nondiabetic patients treated with reperfusion therapy for AMI are limited.

Methods

We investigated long-term clinical outcome in 356 consecutive nondiabetic patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention or thrombolysis as reperfusion therapy. Mean follow-up time was 8 ± 2 years. The patients were divided on the basis of admission glucose level: group 1, <7.8 mmol/L; group 2, 7.8 to 11.0 mmol/L; and group 3, ≥11.1 mmol/L.

Results

Mortality rate in group 1 (n = 163) was 19.0%; in group 2 (n = 151), 26.5%; and in group 3 (n = 42), 35.7% (P < .05). Higher glucose levels were associated with larger enzymatic infarct sizes (P < .01) and more reduced residual left ventricular function (P < .05). Multivariate analysis showed that Killip class >1 at admission (OR, 2.9; 95% CI, 1.7 to 5.0; P < .001), age ≥60 years (OR, 2.4; 95% CI, 1.5 to 4.0, P = .001), thrombolysis as compared with percutaneous coronary intervention (OR, 1.7; 95% CI, 1.1 to 2.7, P = .02), admission glucose category (OR, 1.4; 95% CI, 1.0 to 1.9, P = .04), and anterior location (OR, 1.6; 95% CI, 1.0 to 2.6, 0.03) were independent predictors of long-term clinical outcome.

Conclusions

Elevated admission glucose levels in nondiabetic patients treated with reperfusion therapy for ST-segment elevation myocardial infarction are independently associated with larger infarct size and higher long-term mortality rates.     

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.     

Change of multiple complex coronary plaques in patients with acute myocardial infarction: a study with coronary angiography

Background

Patients with acute myocardial infarction (AMI) may have multiple complex coronary plaques that are not limited to the culprit lesions. However, it is unknown whether they tend to progress in severity, regress, or remain stable. The aim of this angiographic study is to evaluate the natural history of these lesions.

Methods

We consecutively enrolled 229 patients who underwent coronary angiography at the time of their hospitalization to treat AMI with primary angioplasty. Baseline and follow-up (mean follow-up duration, 192 ± 33 days) coronary angiographic data in patients with multiple complex coronary plaques characterized by thrombus, ulceration, plaque irregularity, and impaired flow were compared.

Results

Single complex coronary plaques were identified in 167 patients (73%), and multiple complex plaques were identified in the other 62 patients (27%). Among the patients with multiple complex plaques (62 patients, 83 non-culprit complex plaques), the angiographic examinations were reviewed simultaneously in 43.5% (27 patients, 35 non-culprit complex plaques). Of 35 non-culprit complex lesions, 29 lesions (82%) remained complex without changing into smooth lesions, 1 lesion became totally occluded, and 4 lesions regressed. The severity of non-culprit complex lesions between baseline and follow-up angiography is equal (maximal diameter stenosis, 74% ± 15% vs 72% ± 15%, P = .4). Long-term cardiac events after discharge were more likely to develop in patients with multiple complex plaques than in patients with single complex plaques (24% vs 10%, respectively; P <.01).

Conclusions

In patients with AMI, little angiographic change occurred during 6 months of follow-up in the non-culprit complex plaques.     

Effects of losartan and captopril on left ventricular systolic and diastolic function after acute myocardial infarction: results of the Optimal Trial in Myocardial Infarction with Angiotensin II Antagonist Losartan (OPTIMAAL) echocardiographic substudy

Background

Angiotensin-converting enzyme inhibitors have been shown to attenuate adverse remodeling after acute myocardial infarction (AMI), and the same has been suggested for angiotensin II type 1 receptor antagonists in animal models. Therefore the aim of the study was to compare the effects of losartan and captopril on regional systolic, diastolic, and overall left ventricular (LV) function after AMI.

Methods

Two hundred twenty-five patients aged ≥50 years with documented AMI and heart failure and/or LV dysfunction were randomly assigned treatment with either losartan (50 mg/d) or captopril (50 mg 3 times/d). Echocardiography was performed at randomization and after 3 months; echocardiograms were analyzed blinded at the core laboratory. Main outcome measures were changes in wall motion score index (WMSI), E-wave deceleration time (E-DT), and Tei index of overall LV function.

Results

WMSI decreased in both groups (losartan 1.58 ± 0.23 to 1.52 ± 0.26, P = .009, captopril 1.60 ± 0.24 to 1.48 ± 0.22, P < .001), although the decrease was greater in patients allocated to captopril (captopril −0.12 ± 0.17 vs losartan −0.05 ± 0.19, P = .007). In both groups E-DT increased, although the increase was significant only in patients treated with captoril (193 ± 61 ms to 208 ± 70 ms, P = .05). The change in E-DT was not different between treatment groups (captopril 14 ± 74 ms vs losartan 7 ± 80 ms, P = .52). Tei index decreased in both groups (losartan 0.59 ± 0.13 to 0.55 ± 0.15, P = .04, captopril 0.62 ± 0.15 to 0.55 ± 0.13, P < .001). However, the reduction was significantly greater in patients treated with captopril (captopril −0.08 ± 0.14 vs losartan −0.03 ± 0.14, P = .01).

Conclusion

Losartan and captopril improve systolic and overall LV function after AMI, but the benefit is greater for patients treated with captopril.     

Biomechanical and echocardiographic characterization of flail mitral leaflet due to myxomatous disease: further evidence for early surgical intervention

Background

Flail mitral leaflet (FML) is a common complication of mitral valve prolapse, often leading to severe mitral regurgitation (MR) and left ventricular dysfunction. In the absence of timely surgical correction, survival is significantly impaired. Early recognition of FML and identification of risk factors is important because early intervention increases the chances of survival.

Methods

We studied 123 patients undergoing mitral valve surgery for severe MR caused by myxomatous disease. Chart review, echocardiography, and tensile testing were performed.

Results

Thirty-eight patients had FML, and 85 patients had non-flail mitral leaflet (non-FML). Patients with FML were younger (53.7 ± 1.8 vs 59.3 ± 1.4 years, P = .02), had more severe MR (3.89 ± 0.04 vs 3.76 ± 0.04, P = .02), were less likely to be in New York Heart Association class III or IV heart failure (5% vs 20%, P = .037), and were less likely to have bileaflet mitral valve prolapse (5% vs 38%, P <.001) than non-FML patients. Valve tissue from patients with FML had less stiff chordae (23.5 ± 3.6 vs 59.1 ± 11.7 Mpa, P = .006) that tended to have a lower failure stress (3.8 ± 0.9 vs 9.6 ± 2.2 Mpa, P = .07) and had more extensible leaflets (56.4% ± 7.9% vs 42.9% ± 2.7% strain, P = .04) compared with that of non-FML patients.

Conclusions

The development of FML may result from intrinsic tissue abnormalities and is associated with a distinct subset of the myxomatous population. Identification of such clinical characteristics in this population and knowledge of an implicit mechanical abnormality of valve tissue may further the argument for early surgical correction.     

Comparison of acute changes in left ventricular volume,systolic and diastolic functions,and intraventricular synchronicity after biventricular and right ventricular pacing for heart failure

Background

Biventricular pacing (BiV) therapy has recently been shown to improve systolic function and cause reverse remodeling in patients with advanced heart failure with electromechanical delay. In these patients, the benefit of right ventricular (RV)-based pacing was controversial. We compared the acute changes in systolic and diastolic function, left ventricular (LV) volume, and intraventricular synchronicity in BiV pacing, RV pacing, and without pacing (No) by means of echocardiography and tissue Doppler imaging (TDI).

Methods

TDI was performed in 33 patients with heart failure after undergoing pacemaker implantation, when the device was randomized to BiV, RV, and no pacing modes.

Results

Systolic function was only improved during BiV pacing, but not during RV pacing. This included ejection fraction (No vs RV vs BiV = 24% ± 12% vs 25% ± 10% vs 30% ± 14%, P = .02 vs No), +dp/dt (P = .01), myocardial performance index (P = .01), and isovolumic contraction time (P = .03). Mitral regurgitation was only reduced during BiV pacing (P = .02). LV early diastolic function was depressed in both RV and BiV pacing, as detected by transmitral flow (97 ± 34 vs 80 ± 34 vs 82 ± 32 cm/s, both P ≤ .005) and TDI (mean myocardial early diastolic velocity of 6 basal segments, 3.3 ± 1.7 vs 2.6 ± 1.0 vs 2.6 ± 1.0 cm/s, both P = .01). The LV end-diastolic (187 ± 86 vs 177 ± 84 vs 166 ± 79, P = .003) and end-systolic (146 ± 77 vs 138 ± 79 vs 122 ± 69, P = .003) volumes were only decreased during BiV pacing. For systolic synchronicity, a significant delay in peak systolic contraction in the lateral over the septal wall (171 ± 37 vs 217 ± 46 ms, P = .004) was revealed by TDI when there was no pacing. This was abolished by BiV pacing, in which septal contraction was delayed (195 ± 38 vs 201 ± 53 ms, P = not significant). However, RV pacing restored the lateral wall delay, and systolic asynchrony reappeared (190 ± 40 vs 227 ± 56 ms, P = .01). Diastolic asynchrony between the septal and lateral walls was not evident in these patients and was not affected by either pacing mode.

Conclusion

Only BiV pacing, but not RV pacing, improves systolic function, and reduces mitral regurgitation and LV volumes in patients with heart failure and electromechanical delay. This is attributed to the improvement of systolic synchronicity. Diastolic synchronicity was unaffected, whereas early diastolic function could be jeopardized, by either pacing mode.     

Assessment of respiratory mechanics by impulse oscillometry in orthopneic patients with acute left ventricular failure

Backround

This study investigated the respiratory function and mechanics of patients with orthopnea caused by acute left ventricular failure (ALVF).

Methods

The study comprised 40 patients with ALVF and 15 control subjects. All patients underwent lung function tests and impulse oscillometry in both sitting and supine positions. In a subgroup of 22 patients, isosorbide dinitrate was administered and impulse oscillometry was performed 15 minutes later in the supine position.

Results

No patient reported dyspnea while seated, and the orthopnea score was 2.9 ± 1.4. Left ventricular ejection fraction was 43% ± 10%. Patients demonstrated restrictive spirometric pattern in the sitting position, whereas functional residual capacity was comparable to that of the control group. In the supine position, all pulmonary volumes decreased, except inspiratory capacity which increased. Respiratory reactance (Xrs5) was higher in patients in both sitting (421.8 ± 630.6%pred vs 147.2 ± 72.8%pred, P = .01) and supine (699.8 ± 699.9%pred vs 251.2 ± 151.6%pred, P ≤ .001) positions. Respiratory resistance (Rrs5) (10.6% ± 17.8% mean decrease) and Xrs5 (17.2% ± 39.4% mean decrease) improved after nitrates administration. Orthopnea was better correlated with Xrs5%pred in the supine position (r = .42, P = .007). Ejection fraction was positively correlated with inspiratory capacity %pred (r = .42, P = .007) in the sitting position.

Conclusion

Patients with ALVF demonstrated increased respiratory reactance that correlated with orthopnea severity and improved after nitrates administration.     

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.     

Clinical outcome of percutaneous coronary intervention with antecedent mutant t-PA administration for acute myocardial infarction

Objective

We investigated the acute-phrase and chronic-phase outcomes of patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI) with or without antecedent mutant tissue-type plasminogen (t-PA) administration.

Methods

Thirty-nine patients with a first AMI within 6 hours of onset were randomly assigned to the treatment group (1,600,000 IU IV monteplase, n = 19) or the nontreatment group (n = 20), followed by PCI. Clinical outcomes were then evaluated.

Results

Patient characteristics did not differ between the 2 groups. A significantly higher number of patients in the monteplase group achieved Thrombolysis In Myocardial Infarction trial (TIMI) grade 2 flow or more at the first angiography (84.2% vs 40.0%; P < .005), reduced number of devices (1.44 vs 1.80 devices, P < .05), and reduced procedure times (59.7 vs 86.7 minutes; P < .01), with no differences in peak creatine kinase and rates of major complications and no reflow or distal embolization. Observation over an average of 5.5 months revealed a tendency toward lower target lesion revascularization rates in the monteplase group (17.6% vs 31.6%) but no intergroup difference in rates of major complications. Pretreatment quantitative coronary angioplasty only showed a significant difference in minimal lumen diameter and percent diameter stenosis in the acute phase (1.13 mm in the monteplase group vs 0.66 mm in the nontreatment group, 57.0% vs 73.0%; P < .05). ^99mTc-QGS (quantitative electrocardiographically gated single-photon emission computed tomographic scintigraphy) showed no intergroup differences in left ventricular end-diastolic volume index, end- systolic volume index, and ejection fraction in the acute and chronic phases.

Conclusions

Our results suggest that PCI with antecedent mutant t-PA for AMI not only accelerates reperfusion, thereby facilitating PCI, but also attenuates restenosis in the chronic phase.     

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.     

Primary percutaneous transluminal coronary angioplasty accelerates early myocardial reperfusion compared to thrombolytic therapy in patients with acute myocardial infarction

Background

Successful early reperfusion of the infarcted myocardium as indicated by complete resolution of ST-segment elevations has been shown to be associated with an improved outcome in patients with acute ST-elevation myocardial infarction (AMI). The aim of this study was to compare early ST resolution in patients treated with primary percutaneous transluminal coronary angioplasty (PTCA) or thrombolytic therapy for AMI.

Methods

A total of 1379 patients with AMI whose symptoms began <6 hours previously were enrolled in the Evaluation of the Safety and Cardioprotective effects of eniporide in Acute Myocardial Infarction (ESCAMI) trial and treated with primary PTCA (n = 528) or thrombolytic therapy (n = 851). Twelve-lead electrocardiograms (ECG) were obtained at baseline, directly after PTCA and at 90 minutes after the initiation of thrombolytic therapy.

Results

There were no differences with respect to clinical or ECG baseline variables between the 2 groups. The time intervals between hospital admission and ECG 2 (obtained 0-30 min after PTCA and 90 min after start of thrombolysis) were 121 ± 62 minutes in the PTCA group and 137 ± 57 minutes in the thrombolysis group, respectively. In ECG 2, complete (≥70%) ST resolution was observed more often in the PTCA treated patients (35 vs 27%, P = .003). The incidence of congestive heart failure until 6 weeks was lower in the PTCA group (11.2% vs 17.6, P = .001). Mortality after 6 weeks (3.4% vs 5.6%, P = .07) and after 6 months (4.5% vs 7.1%, P = .06) tended to be lower in the PTCA group.

Conclusion

Primary PTCA compared to thrombolytic therapy is associated with an accelerated myocardial reperfusion within 90 minutes after the start of reperfusion therapy. This early advantage in myocardial reperfusion is associated with an improved clinical outcome.     

Impact of early, late, and no ST-segment resolution measured by continuous ST Holter monitoring on left ventricular ejection fraction and infarct size as determined by cardiovascular magnetic resonance imaging

Background

The goal of this study is to determine the predictive value of ST-segment resolution (STR) early after percutaneous coronary intervention (PCI), late STR, and no STR for left ventricular ejection fraction (LVEF) and infarct size (IS) by cardiovascular magnetic resonance (CMR) at follow-up in patients with ST-segment elevation myocardial infarction.

Methods

The analysis included 199 patients who were enrolled in the PRoximal Embolic Protection in Acute myocardial infarction and Resolution of ST-Elevation trial and in whom both continuous ST Holter and CMR at follow-up were available. Patients were stratified into 3 groups: (1) early complete (≥70%) STR measured immediately after last contrast injection (n = 113); (2) late complete STR (n = 52), defined as complete STR from 30 to 240 minutes after PCI; and (3) no complete STR after 240 minutes (n = 34).

Results

Patients with early STR had more preserved LVEF and smaller IS compared to patients with late STR or no STR (LVEF: early STR, 54% ± 8%; late STR, 46% ± 13%; no STR, 43% ± 11%; and IS: 3.9 ± 3.3 g/m²; 8.0 ± 6.9 g/m²; 12.0 ± 6.0 g/m²; respectively; all P < .0001). Early STR was independently predictive for LVEF (β = 8.5; P = .0005) and IS (β = −7.0; P < .0001). Late STR was not predictive for LVEF (β = 1.6; P = .51) but predictive for IS (β = −3.5; P = .003).

Conclusions

Patients with early complete STR after primary PCI have better preserved LVEF and smaller IS. Patients with late complete STR do not have better preserved LVEF but do have smaller IS. ST-segment resolution is a strong, independent predictor of LVEF and IS as assessed by CMR.     

Subcutaneous enoxaparin with early invasive strategy in patients with acute coronary syndromes

Background

Subcutaneous enoxaparin during at least 48 hours provides adequate anticoagulation and good clinical results in patients with non-ST-segment elevation acute coronary syndromes undergoing percutaneous coronary intervention (PCI).

Methods

In this nonrandomized retrospective study, we compared 347 patients with non-ST-segment elevation acute coronary syndromes who underwent rapid PCI after only 2 injections of subcutaneous enoxaparin (EI, n = 117) to those referred later to the catheterization laboratory with ≥3 injections (DI, n = 230). We measured anti-Xa at the time of PCI and evaluated bleeding and major ischemic events (death/myocardial infarction) at 30 days.

Results

Patients in the EI group more frequently received glycoprotein IIb/IIIa inhibitors and clopidogrel preceding PCI than did patients in the DI group (58.1% vs 31.7%, P < .0001 for glycoprotein IIb/IIIa inhibitors and 68.4% vs 40.4% for clopidogrel pretreatment, P < .0001, respectively). The anti-Xa activity measured at the time of catheterization (0.92 ± 0.04 U/mL vs 0.96 ± 0.02 U/mL, EI vs DI, P = .25) and the injection-to-catheterization times (5.6 ± 0.2 h vs 5.2 ± 0.1 h, EI vs DI, P = .17) were similar in both groups. The 30-day bleeding rates of 1.7% and 4.8% in the EI and DI strategies were found to be equivalent with a significant non-inferiority test for the EI strategy (P < .05). There was a nonsignificant trend for less death or myocardial infarction at 30 days in the EI group compared to the DI group (4.3% vs 7.0%, non-inferiority test not significant).

Conclusion

A rapid invasive strategy with only 2 subcutaneous injections of enoxaparin provides similar levels of anticoagulation, and is associated with a favorable trend for ischemic events and with safety equivalent to a more prolonged “upstream” treatment with enoxaparin.     

Electrocardiographic prediction of short-term prognosis in patients with acute myocardial infarction associated with the left main coronary artery

Purpose

The purpose of this study was to assess the usefulness of electrocardiogram on admission to predict short-term prognosis in patients with acute myocardial infarction (AMI) associated with left main coronary artery (LMCA).

Methods

Electrocardiogram was obtained on admission in 41 patients with AMI associated with LMCA who underwent reperfusion therapy. Electrocardiographic findings were compared between nonsurvivors and survivors.

Results

There were 24 nonsurvivors and 17 survivors during 30-day follow-up. Nonsurvivors had ST-segment elevation in both leads aVR and aVL (54% vs 18%, P < .05), left anterior fascicular block (83% vs 41%, P < .05), and right bundle-branch block (54% vs 18%, P < .05) more frequently, and ST-segment depression in lead V₅ (17% vs 59%, P < .05) less frequently than survivors among patients with AMI associated with LMCA.

Conclusions

Our data suggested that electrocardiogram on admission might be useful to predict short-term prognosis in patients with AMI associated with LMCA.     

Association of the PURSUIT risk score with predischarge ejection fraction, angiographic severity of coronary artery disease, and mortality in a nonselected, community-based population with non-ST-elevation acute myocardial infarction

Background

The Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) risk score was derived from the PURSUIT trial population for 30-day mortality prediction.

Methods

The PURSUIT risk score was calculated for 337 consecutive Olmsted County residents with non-ST-elevation acute myocardial infarction admitted to the coronary care unit of our institution from 1988 through 1998. Predischarge ejection fraction (EF) measurement was available for 246 patients (73%). After excluding patients with prior coronary artery bypass graft surgery (n = 42), 219 patients (65%) had coronary angiography within 30 days of admission. Mortality at 30 days was 8.9%. Among 30-day survivors, mortality at 1 year was 7.9%.

Results

Mean age was 70 ± 13 years, and 37% of patients were women. Mean predischarge EF was 52% ± 16%. Patients with higher PURSUIT risk score had lower EF (P < .001). Three-vessel (≥70% stenosis in all 3 coronary arteries) or left main (≥50% stenosis) coronary artery disease was present in 60 of 219 patients (27%) who had coronary angiography. Higher PURSUIT risk score was associated with greater likelihood of 3-vessel or left main disease (P < .001). The PURSUIT risk score had very good predictive accuracy for both early (30-day, C-statistic = 0.78) and late (30-day to 1-year, C-statistic = 0.77) mortality.

Conclusions

The PURSUIT risk score correlates with EF, angiographic severity of coronary artery disease, and short- and long-term mortality of nonselected patients with non-ST-elevation acute myocardial infarction.     

Quantitative regional wall motion analysis with early contrast ventriculography for the assessment of myocardium at risk in acute myocardial infarction

Background

Several techniques have been used to quantify the myocardium at risk, including measurement of regional ventricular function with contrast ventriculography and measurement of perfusion defect size with tomographic technetium-99m-sestamibi imaging. This study evaluates the correlation between these 2 techniques.

Methods

Twenty-three patients with angiographically documented coronary occlusion and acute myocardial infarctions (10 anterior, 13 inferior) were studied. All patients had contrast left ventriculography at the time of their acute angiogram before any revascularization therapy. Regional wall motion parameters measured with the centerline method were the severity, circumferential extent, and global circumferential extent of hypokinesis and the mean standardized motion in predefined areas. Technetium-99m-sestamibi was injected before reperfusion therapy with measurement of the myocardium at risk using single photon emission computed tomography imaging.

Results

The tomographic sestamibi-measured myocardium at risk was significantly greater for anterior infarctions compared with inferior infarctions (40% ± 18% vs 14.0 ± 8.5%, P = .0001). The only parameter of regional wall motion to show a significant difference by infarct location was global circumferential extent of hypokinesis (43% ± 25% vs 22% ± 15%, P = .02). The other parameters were not significantly different between anterior and inferior myocardial infarctions. For anterior infarctions, these parameters of regional wall motion correlated with myocardium at risk assessed with sestamibi: global circumferential extent of hypokinesis (r = .88, P < .01), circumferential extent of hypokinesis (r = .78, P < .01), mean standardized motion in predefined areas (r = -.74, P < .05), and severity of hypokinesis (r = -.70, P < .05). For inferior infarctions, there was no significant correlation between any of these parameters of regional wall motion and myocardium at risk assessed with sestamibi imaging.

Conclusion

The assessment of regional ventricular function with contrast ventriculography correlates with the area of myocardium at risk measured with tomographic technetium-99m-sestamibi for anterior, but not for inferior, myocardial infarctions. Therefore, these parameters of regional wall motion are a poor measure of the efficacy of reperfusion therapies.     

Effects of oral amino acid supplementation on myocardial function in patients with type 2 diabetes mellitus

Background

Diabetes mellitus is associated with an increased rate of cardiac amino acid catabolism that could interfere with cardiac function.

Methods

We assessed the effects of an oral amino acids mixture (AAM) on myocardial function in patients with type 2 diabetes mellitus (DM2). We studied 65 consecutive patients with DM2 who had normal resting left ventricular ejection fraction (LVEF) and did not have obstructive coronary artery disease (CAD). After baseline evaluations, patients were randomized to receive, in a single-blinded fashion, AAM (12 grams/day) or placebo for 12 weeks, after which, treatment was crossed over for another similar period. At baseline and at the end of each treatment, 2-dimensional ecocardiography at rest and during isometric exercise (handgrip) was performed, as were biochemical assays. Twenty adults, matched for age, sex, and body mass index served as control subjects.

Results

At baseline and during AAM or placebo treatment, resting left ventricular dimensions and LVEF in patients with DM2 did not differ from those of control subjects. In patients with DM2, at baseline and during placebo treatment, peak handgrip LVEF decreased significantly in comparison with the resting value (63% ± 9% vs 56% ± 9%, P <.001; and 62% ± 6% vs 55% ± 8%, P <.001). During AAM treatment, peak handgrip LVEF did not differ from resting value (66% ± 11% vs 64% ± 9%, P = not significant). Thus, exercise LVEF was higher during AAM treatment than both baseline and placebo treatment (66% ± 11% vs 56% ± 9% and vs 55% ± 8%, P <.001). In contrast to placebo treatment, after the AAM supply, a decreased glycated hemoglobin level was observed (7.0% ± 1.3% vs 7.6% ± 1.8%, P <.05).

Conclusions

Myocardial dysfunction is easily inducible with isometric exercise in patients with DM2 who have normal resting LV function and do not have CAD. An increased amino acid supply prevents this phenomenon and improves metabolic control.