Prognostic significance of inverse spatial QRS-T angle circadian pattern in myocardial infarction survivors

Background

We investigated the predictive value of the spatial QRS-T angle (QRSTA) circadian variation in myocardial infarction (MI) patients.

Methods

Analyzing 24-hour recordings (SEER MC, GE Marquette) from 151 MI patients (age 63 ± 12.7), the QRSTA was computed in derived XYZ leads. QRS-T angle values were compared between daytime and night time. The end point was cardiac death or life-threatening ventricular arrhythmia in 1 year.

Results

Overall, QRSTA was slightly higher during the day vs. the night (91° vs. 87°, P = .005). However, 33.8% of the patients showed an inverse diurnal QRSTA variation (higher values at night), which was correlated to the outcome (P = .001, odds ratio 6.7). In multivariate analysis, after entering all factors exhibiting univariate trend towards significance, inverse QRSTA circadian pattern remained significant (P = .036).

Conclusion

Inverse QRSTA circadian pattern was found to be associated with adverse outcome (22.4%) in MI patients, whereas a normal pattern was associated (96%) with a favorable outcome.     

Association between plasmin activation system and intravascular ultrasound signs of plaque instability in patients with unstable angina and non-st-segment elevation myocardial infarction

Background

The association between intravascular ultrasound (IVUS) signs of plaque instability and plasma levels of biomarkers was determined in patients with unstable angina and non-ST-segment elevation myocardial infarction (UA/NSTEMI).

Methods

Fifty-two patients underwent coronary angiography and IVUS 8 ± 5 hours after the onset of chest pain. IVUS analysis included plaque morphology, disruption, thrombi and eccentricity, lumen, external elastic membrane, and plaque plus media areas of culprit lesion and reference segments and arterial remodeling. Plasma levels of the thrombin activation system (thrombin-antithrombin complex [TAT], tissue factor pathway inhibitor [TFPI], and prothrombin fragments 1+2 [F1+2]) and plasmin activation system (tissue and urokinase-type plasminogen activator [t-PA and u-PA], plasminogen activator inhibitor-1 [PAI-1], and D-dimer) were measured with enzyme-linked immunosorbent assay kits before angiography.

Results

Elevated levels of TAT (7.2 ± 6.0 μg/L), F1+2 (1.8 ± 1.0 nmol/L), TFPI (179.1 ± 131.0 ng/mL), PAI-1 (95.4 ± 54.6 ng/mL), t-PA (10.6 ± 8.8 ng/mL), and u-PA (2.6 ± 0.9 ng/mL) were found in patients with UA/NSTEMI. The serum levels of D-dimer (40.0 ± 39.5 ng/mL) remained in reference range. Expansive and constrictive remodeling were found in 18 (35%) and 12 (23%) patients, respectively. Expansive remodeling of the culprit lesion was associated with significantly higher plasma levels of PAI-1 (121.6 ± 55.0 vs 87.7 ± 61.5 and 77.4 ± 42.8 ng/ml, P = .039), and u-PA (3.0 ± 1.2 vs 2.2 ± 0.5 and 2.5 ± 0.7 ng/mL, P = .026) as compared with constrictive and neutral remodeling. Increased plasma levels of u-PA were associated with plaque rupture (3.0 ± 0.7 vs 2.5 ± 0.9 ng/mL, P = .062). Plasma levels of PAI-1 and u-PA correlated positively with plaque plus media (P = .0297 and P = .0093) and external elastic membrane areas (P = .010 and P = .0002).

Conclusions

Elevated levels of biomarkers of plasmin activation system are associated with signs of plaque instability of culprit lesion in UA/NSTEMI and might therefore serve as non-invasive determinants of the population that is at high risk for subsequent adverse events.     

Comparison of the correlation of the Selvester QRS scoring system with cardiac contrast-enhanced magnetic resonance imaging-measured acute myocardial infarct size in patients with and without thrombolytic therapy

Background

After an acute myocardial infarction (MI), it is important to define the infarct size because it is related to mortality and morbidity. The Selvester QRS Score is an electrocardiographic (ECG) method that has been developed for estimating MI size. It has been shown to correlate well with postmortem anatomically measured sizes of single MI in patients who did not receive thrombolytic therapy. The aim of this study was to test the hypothesis that correlation between Selvester QRS Score-estimated MI size and contrast-enhanced magnetic resonance imaging (ceMRI)-measured MI size is equivalent in patients who did vs those who did not receive thrombolytic therapy.

Methods

Thirty-six patients with MI (24 with thrombolytic therapy and 12 without) received ceMRI and ECG at admission and at 1 or 6 months after admission. Indeed, in 23 of the patients, the therapy was intravenous only. The Selvester QRS Score was calculated using the 1-month ECG or, if not available, the 6-month ECG. The correlation between the 2 measures of MI size was determined for all patients and for the 2 groups separately.

Results

The mean MI size in the group that did not receive thrombolytic therapy was 8.5% ± 6.4% estimated by the Selvester QRS Score and 11.7% ± 10.2% measured by ceMRI. For the group that received thrombolytic therapy, Selvester QRS Score was 13.9% ± 11.1% and ceMRI was 20.2% ± 11.3%. The mean MI size in both groups combined was 12.1% ± 10.0% estimated by the Selvester QRS Score and 17.3% ± 11.5% measured by ceMRI. The Spearman rank correlation coefficient between Selvester QRS Score and ceMRI was 0.74 (P < .0001) for all patients, 0.74 (P < .0001) for the group that received thrombolytic therapy, and 0.64 (P = .024) for the group that did not receive thrombolytic therapy.

Conclusions

The associations between Selvester QRS Score and ceMRI-based MI were statistically significant and similar in both groups.     

Tissue Doppler atrial conduction times and electrocardiogram interlead P-wave durations with varying severity of obstructive sleep apnea

Objectives

Obstructive sleep apnea (OSA) has been reported to be associated with an increased risk of atrial fibrillation. The aim of this study was to investigate atrial electromechanical couplings in patients with OSA and the relationship between these parameters and P-wave dispersion (Pd).

Methods

One hundred twenty-six patients were enrolled in this study. All patients underwent polysomnographic examination. The apnea-hypopnea index (AHI) was defined as the number of apneas and hypopneas per hour of sleep. An AHI score of 5 or more was diagnosed as OSA, and an AHI score of less than 5 was diagnosed as OSA (−). Thirty-nine of the patients had an AHI score of less than 5 (group 1), 42 of the patients had AHI score between 5 and 30 (mild and moderate, group 2), 45 of the patients had an AHI score more than 30 (severe, group 3). Atrial electromechanical coupling (PA), intra-atrial, and interatrial electromechanical delay were measured with tissue Doppler imaging. P-wave dispersion was calculated from 12-lead electrocardiogram.

Results

Maximum P-wave duration was higher in group 3 compared with groups 2 and 1 (126.0 ± 16.7 vs 111.0 ± 12.5 [P < .001] and 126.0 ± 16.7 vs 99.9 ± 10.0 [P < .001], respectively). Maximum P-wave duration was higher in group 2 than in group 1 (111.0 ± 12.5 vs 99.9 ± 10.0, P < .001). P-wave dispersion was higher in group 3 compared with groups 2 and 1 (50.9 ± 11.5 vs 37.0 ± 8.6 [P < .001] and 50.9 ± 11.5 vs 27.9 ± 6.8 [P < .001], respectively). P-wave dispersion was higher in group 2 than in group 1 (37.0 ± 8.6 vs 27.9 ± 6.8, P < .001). Minimum P-wave duration did not differ between the groups. Atrial PA at the left lateral mitral annulus (lateral PA), septal mitral annulus (septal PA), and right ventricular tricuspid annulus (RV PA) were significantly higher in group 3 than in group 2 (P < .001, P = .001, and P = .009, respectively). Lateral PA, septal PA, and RV PA were higher in group 2 compared with group 1 (P < .001, P = .003, and P = .009, respectively). Interatrial electromechanical delay (lateral PA − RV PA) was significantly longer in group 3 compared with groups 2 and 1 (33.6 ± 12.1 vs 22.4 ± 9.4 [P < .001] and 33.6 ± 12.1 vs 14.9 ± 9.2 [P < .001], respectively). Interatrial electromechanical delay was longer in group 2 than in group 1 (22.4 ± 9.4 vs 14.9 ± 9.2, P = .001). There was a positive correlation between AHI and Pd, lateral PA, septal PA, RV PA, interatrial electromechanical delay, and left-sided intra-atrial electromechanical delay.

Conclusion

Prolongation of electromechanical delay and increased Pd are associated with apnea-hypopnea index (AHI) and hence the severity of disease.     

Aortic root dysfunctioning and its effect on left ventricular function in Ross procedure patients assessed with magnetic resonance imaging

Background

This study evaluated the diameters and distensibility of the aortic root as well as the degree of aortic regurgitation (AR) and its effect on left ventricular (LV) function in patients 8.2 ± 3.1 years after they underwent the Ross procedure, with a comparison of these parameters between patients and matched healthy subjects.

Methods

Eighteen Ross procedure patients (16 male patients, age [mean ± SD] 19.2 ± 3.8 years) and 18 matched healthy subjects (16 male patients, age [mean ± SD] 19.7 ± 4.2 years) underwent magnetic resonance imaging. Measurements for diameters (at 4 levels) and the distensibility of the aortic root were performed using a steady-state free precession sequence. Aortic flow was assessed with a velocity-encoded phase-contrast sequence. Left ventricular systolic function was assessed with a gradient-echo sequence in the short-axis plane. Comparison of parameters was performed using the Mann-Whitney U test. Correlations between diameters, distensibility, AR fraction, and LV systolic function were expressed with Spearman rank correlation coefficients. Linear regression analysis was used to identify predictors of LV systolic dysfunction.

Results

Aortic root diameters were increased in Ross procedure patients as compared with healthy subjects (mean difference 6.3-11.6 mm, P ≤ .02 at all 4 levels). Distensibility of the aortic root was lower in patients (1.9 ± 1.1 vs 7.8 ± 3.3 mm Hg⁻¹, P < .01). An AR fraction >5% was present in 14 of the 18 patients (mean AR fraction 8% ± 5% vs 1% ± 1%, P < .01). Left ventricular ejection fraction was lower in patients (50% ± 6% vs 57% ± 6%, P < .01). Dilatation, decreased distensibility, and AR fraction were correlated with impaired LV systolic function (P < .05 for all). The AR fraction predicted impaired LV systolic function (P < .01).

Conclusions

Magnetic resonance imaging shows dilatation and decreased distensibility of the aortic root, AR, and consequent impaired LV systolic function in patients after the Ross procedure.     

The new universal definition of myocardial infarction criteria improve electrocardiographic diagnosis of acute coronary syndrome

Introduction/Methods

To assess whether revised electrocardiographic (ECG) criteria improve emergency department identification of patients with acute myocardial infarction (MI) or unstable angina (UA) and predict outcome, we studied 120 patients with a nondiagnostic initial ECG by prior criteria. Electrocardiograms were read in a blinded fashion months apart with standard and then revised criteria, and analyzed by χ² and logistic regression analysis.

Results

In 12 subjects (10%), the initial ECG was now interpreted as diagnostic of ischemia. Eleven (92%) had an MI, 1 had UA (8%), and none had a noncardiac diagnosis. Ischemic ECG changes were strongly associated with MI or UA (P = .003). At 1-year follow-up, ECG changes diagnostic of ischemia were associated with a trend toward higher mortality (25% vs 7%, P = .07), but after adjustment for clinical factors, ECG changes were not an independent predictor of 1-year mortality.

Conclusions

Revision of the ECG criteria for ischemia was associated with enhanced diagnostic performance and identified a subset of patients at higher risk.     

Comparative evaluation of the usability of 2 different methods to perform mild hypothermia in patients with out-of-hospital cardiac arrest

Background

Several studies have shown that mild hypothermia (32-34 °C) markedly mitigates brain damage after cardiac arrest (CA). This study aimed to compare the efficacy of the non-invasive cooling device Hilotherm® Clinic (Hilotherm® GmbH, Germany) with conventional cooling to induce and maintain mild hypothermia in patients after out-of-hospital CA.

Methods

50 adult patients with an indication for controlled mild hypothermia were prospectively assigned to conventional cooling (n = 20) or cooling with the Hilotherm system (n = 30). Patients receiving a cooling therapy by Hilotherm were treated either with 0.35 m² (n = 20) or with 0.7 m² (n = 10) surface area of cooling sleeves.

Results

The speed of cooling was significantly higher in both Hilotherm groups compared to conventional cooling (Hilotherm 0.7 m²: 0.91 ± 0.08 °C/h, Hilotherm 0.35 m²: 0.47 ± 0.04 °C/h, and conventional: 0.3 ± 0.04 °C/h, p ≤ 0.003). Temperature deviation from the target temperature of 33 °C was significantly higher in the conventional group compared to both Hilotherm groups. During induction of mild hypothermia a significant reduction of the mean arterial blood pressure and the heart rate was observed without significant differences between the groups. However, the speed of cooling (range 0.3-0.91 °C/h) did not correlate to the decrease of blood pressure and heart rate. Norepinephrine dosing during induction of mild hypothermia and re-warming (1st-2nd day) was significantly increased compared to the 3rd day after admission in all groups. Dobutamine dosing and 30 days in-hospital mortality did not differ significantly between the groups.

Conclusions

Rapid and reliable mild hypothermia can be better achieved by the non-invasive cooling system Hilotherm compared to conventional cooling with ice packs and cold infusion.     

Regional differential expression of TREK-1 at left ventricle in myocardial infarction

Background

Altered membrane electrophysiology contributes to arrhythmias after myocardial infarction (MI). TREK-1 channel is essential in various physiological and pathological conditions through its regulation on resting membrane potential and voltage-dependent action potential duration.

Objectives

The aim of this study was to investigate changes in gene expression and electrophysiology of TREK-1 in the left ventricle in a MI model.

Methods

Fifty-five rats were divided into 5 groups: sham-operated group, 6 hours, 24 hours, 3 days, and 7 days post MI group (n = 11 per group). TREK-1 messenger RNA (mRNA) expression level in the infarct region (IR) and infarct border region (IBR) were quantified by real-time polymerase chain reaction (PCR), and TREK-1 current density at the IBR was recorded with whole-cell patch-clamp technique.

Results

TREK-1 mRNA expression decreased significantly in both endocardial and epicardial cells in the infarct region after MI. Conversely, TREK-1 increased significantly in endocardial and epicardial cells from the IBR (P < 0.01). Current density of TREK-1 at IBR increased significantly in both epicardial and endocardial cells after MI (P < 0.01).

Conclusions

TREK-1 demonstrates specific changes in expression and electrophysiological function in left ventricle post MI. These results suggest that TREK-1 may participate in pathophysiologic alteration and electrical remodelling of left ventricular myocardium after MI, which may eventually lead to post-MI ventricular arrhythmias.     

Myocardial alterations in the murine model of fabry disease can be reversed by enzyme replacement therapy

Background

Fabry disease results from deficiency of alpha-galactosidase A (AGA), causing lysosomal storage of globotriaosylceramide in heart and other tissues. Since 2003, enzymatic replacement therapy with recombinant AGA agalsidase alfa (R-AGA) was approved for clinical use.

Methods

We evaluated whether, in mice knocked out for AGA (FM, n = 31), the myocardium was altered with respect to the wild-type mice (WT, n = 25) and whether alterations were reversed in FM treated with intravenous R-AGA, 0.5 mg/kg every other week during 2 months (FM-AGA, n = 12).

Results

Left ventricular (LV) contractility was depressed in FM, evaluated by LV ΔP/Δt (FM = 2832 ± 85 mm Hg/s, WT = 3179 ± 119 mm Hg/s; P < 0.05), papillary muscle contraction (FM = 39.8 ± 17.3 mg, WT = 67.5 ± 15.7 mg; P < 0.05), or shortening fraction measured by M-mode echocardiography (FM = 30% ± 6%, WT = 47% ± 2%; P < 0.05). LV stiffness (arrested hearts) decreased in FM (FM = 35.57 ± 3.5 mm Hg/20 μl; WT = 68.86 ± 6.12 mm Hg/20 μl; P < 0.05). FM myocytes showed augmented size, disorganized architecture, and intracytoplasmic vacuolization. Alterations reverted in FM-AGA: LV ΔP/Δt = 3281 ± 456 mm Hg/s and LV stiffness = 58.83 ± 2.15 mm Hg/20 μl, with normalization of myocyte architecture. No reversion was detected with AGA solvent.

Conclusions

The FM represent a mild, early stage of the disease, since myocardial alterations are not prominent and appear in nonhypertrophic hearts. Reversion of alterations in the FM-AGA suggests that enzymatic replacement therapy can be useful when administered in early stages of this disease.     

Characterization of ischemic colitis associated with myocardial infarction: an analysis of 23 patients

Purpose

The study characterizes the clinical presentation of ischemic colitis (IC) associated with myocardial infarction (MI) and helps determine whether the primary mechanism for this association is thrombus, embolus, or localized nonocclusive mesenteric ischemia (NOMI) associated with systemic hypotension.

Methods

We compared 23 study patients presenting with IC occurring simultaneously with or within 3 days after MI who were admitted to 5 medical centers versus (1) 32 patients with IC without MI (IC-controls) or (2) 32 patients with MI without IC (MI-controls).

Results

Of 17,500 patients admitted to the study sites with MI, 23 (0.13%) had IC. Study patients had a high in-hospital mortality of 39%. An Acute Physiology and Chronic Health Evaluation (APACHE) II score greater than 15 was a significant predictor of mortality in these patients (P<.04). Compared with the IC-controls, study patients had a significantly lower mean arterial pressure (MAP) (76.0 ± 17.1 mm Hg vs 98.3 ± 18.6 mm Hg, P<.0001) and a significantly higher rate of hypotension (57% vs 9%, odds ratio [OR] = 12.6, confidence interval [CI]: 3.10-49.7, P<.001). The 2 groups, however, had a similar mean number of risk factors for thromboembolism per patient. Study patients had more severe illness than IC-controls, as demonstrated by mean APACHE II scores (19.0 ± 5.5 vs 10.4 ± 4.8, P<.0001). Study patients had a significantly higher incidence of complications, including respiratory failure (57% vs 13%, P=.001), altered mental status (48% vs 13%, P<.01), and renal insufficiency or failure (61% vs 28%, P<.04). Study patients had a significantly lower minimum hematocrit. Study patients had a significantly higher rate of prolonged hospitalization (>30 days) or in-hospital death (74% vs 19%, OR = 12.3, CI: 3.47-43.5, P<.0001). Compared with MI-control patients, study patients had a significantly lower MAP, significantly higher rate of hypotension, much higher mean APACHE II score, much higher incidence of complications, and significantly worse hospital outcome.

Conclusions

Patients with both IC and MI present as a clinically distinct group from patients with either IC alone or MI alone. They have significantly more complications and worse in-hospital prognoses. They present with a dramatically lower MAP and a higher frequency of hypotension. This last finding suggests that the most common and most important mechanism for IC with MI may be hypotension from cardiogenic shock. Hypotension is the cardinal risk factor for generalized NOMI with acute mesenteric ischemia and may be an important risk factor for localized NOMI with IC. An APACHE II score greater than 15 may be a predictor of mortality from IC after MI.     

Plaque blush,branch location,and calcification are angiographic predictors of progression of mild to moderate coronary stenoses

Background

Angiographic predictors of plaque progression are weak and few: length, irregular surface, turbulence, low shear, and (in some studies) eccentricity and calcification. Having noted plaques that briefly retained dye after angiography, we interpreted these as plaques with a fissured surface or neovascularization and hypothesized that progression would be predicted by “plaque blush.”

Methods

Plaques (<50% diameter stenosis) in 68 pairs of angiograms, 5.6 ± 4.8 months apart, were reviewed by 2 blinded observers. The presence of plaque blush, calcification, clot (mobile defect), eccentricity, and a branch point location were compared between progressing (≥20% stenosis increase) and nonprogressing plaques.

Results

Sixteen lesions in 15 patients progressed from 29% ± 13% to 68% ± 14% over a period of 8.1 ± 7.9 months. Patients with and without progression were similar in sex, age, congestive heart disease risk factors, medications, interval between angiograms, clinical presentation, and initial stenosis severity. By logistic regression, plaque blush (BL) (P = .002), calcification (CA) (P = .024), and a branch (BR) point location (P = .001) predicted plaque progression. The odds ratio for plaque progression (ORp) was calculated as ORp = e^{2.5 × BL + 1.8 × CA + 2.6 × BR}. Using an ORp of 1/3, the model has 81% sensitivity and 77% specificity. A second analysis in which each progressive lesion was compared with proximal and distal lesions and with one in a different coronary artery yielded similar results.

Conclusions

In mild to moderate coronary stenoses, studied retrospectively, plaque blush (a new sign) and a branch point location were strong predictors of plaque progression, whereas calcification was a weak predictor of progression.     

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.     

The relationship between serial postinfarction T wave changes and infarct size and ventricular function as determined by cardiac magnetic resonance imaging

Background

The value of sequential T wave changes on the electrocardiogram (ECG) has less well been described than ST-segment changes in the follow-up of patients with myocardial infarction (MI). We investigated whether the amplitude of T wave positivity correlates with infarct size (IS) and left ventricular ejection fraction (LVEF) measured using cardiac magnetic resonance imaging 3 months after reperfusion therapy.

Materials and Methods

Fifty-five patients with a first acute MI referred for primary percutaneous coronary intervention were included. Electrocardiograms were analyzed within 4 hours after reperfusion and at 3 months, measuring T wave ampitudes in 2 contiguous infarct-related leads, summed up as one value called T wave amplitude. Cardiac magnetic resonance imaging was performed at 3 months of follow-up. Correlations between T wave amplitude, IS, and LVEF were tested with Pearson r correlation coefficient test. Subanalyses were performed using a 2-sample t test.

Results

A good correlation was found between LVEF and IS (r = −0.7, P < .0001). Most of the patients had inferior MI location (69%). In this group, there were significant positive correlations between the amount of T wave positivity and both IS (r = −0.40, P = .012) and LVEF (r = 0.33, P = .043). Results were similar in patients with and without an increase in T wave amplitude during follow-up.

Conclusions

In this study of patients with reperfused MI, patients with inferior locations demonstrated a statistically significant relationship between the amount of positivity of T wave amplitude and both IS and LVEF measured at 3 months. Furthermore, these results were independent of whether the T wave positivity was persistent or evolutionary between the immediate postreperfusion and 3-month ECG recordings.     

The evaluation of an electrocardiographic myocardial ischemia acuteness score to predict the amount of myocardial salvage achieved by early percutaneous coronary intervention : Clinical validation with myocardial perfusion single photon emission computed tomography and cardiac magnetic resonance

Background

The time from symptom onset to reperfusion in acute myocardial infarction (MI) has been shown to be a poor predictor of patient outcome. Acute electrocardiographic (ECG) changes, however, have been shown useful for estimated acuteness of myocardial ischemia using the Anderson-Wilkins ECG ischemia acuteness score (AW-acuteness score). The aim was to study whether acute ischemic ECG changes can predict the amount of salvageable myocardium in patients with acute ST-elevation MI.

Methods

Thirty-eight patients treated with primary percutaneous coronary intervention for first-time ST-elevation MI were retrospectively enrolled. Myocardium at risk (MaR) was determined by myocardial perfusion single photon emission computed tomography acutely or by T2-weighted cardiac magnetic resonance after 1 week, at the same time when final MI size was determined by late gadolinium enhancement. Myocardial salvage was calculated as (MaR − MI size)/MaR and compared with AW-acuteness score and time from symptom onset to primary percutaneous coronary intervention.

Results

The AW-acuteness score correlated significantly with salvageable myocardium for right coronary artery (RCA) occlusions (r = −0.57; P = .02) but not for left anterior descending artery (LAD) occlusions (r = −0.04; P = .88). Time from symptom onset did not correlate with the amount of salvageable myocardium (LAD, r = 0.04 and P = .87; RCA, r = −0.40 and P = .13).

Conclusions

There is a moderate correlation between AW-acuteness score and salvageable myocardium in patients with acute RCA occlusion but not in patients with LAD occlusion.     

Early and long-term outcomes after percutaneous coronary intervention of unprotected left main coronary disease with drug-eluting stents in patients with non-ST-elevation acute coronary syndrome

Background

Patients presenting with non-ST-elevation acute coronary syndrome (NSTE-ACS) and unprotected left main coronary disease (ULMCD) are among the highest risk patients but current consensus guidelines do not address the optimal timing and mode of revascularization for these individuals.

Methods

In this single-centre registry, we evaluated the clinical outcomes of 151 consecutive patients with NSTE-ACS and ULMCD who underwent percutaneous coronary intervention with drug-eluting stents from 2005 to 2009.

Results

Overall in-hospital major adverse cardiac event (MACE) rate was 5.3%, mortality rate was 0.7%. At 30 months ± 15 months, 30 patients (19.9%) experienced MACE. The 4-year cumulative survival rate of no MACE was 73.2% and cumulative survival rate was 90.6%. Left ventricular ejection fraction (hazard ratio [HR] 0.947; 95% confidence interval [CI], 0.898-0.998; P = 0.043) and SYNTAX [SYNergy between percutaneous coronary intervention with TAXus and cardiac surgery] score ≥ 33 (HR 1.28; 95% CI, 1.025-1.433; P = 0.029) were associated with MACE, while only left ventricular ejection fraction (HR 0.82; 95% CI, 0.69-0.973; P = 0.023) was associated with mortality.

Conclusions

Our study demonstrates the feasibility of percutaneous coronary intervention with drug-eluting stents in patients with NSTE-ACS and ULMCD. The early and long-term outcomes were acceptable. Left ventricular ejection fraction and SYNTAX score ≥ 33 predict MACE and only left ventricular ejection fraction predicts mortality.     

Beneficial effects of angiotensin-converting enzyme inhibitor and nitrate association on left ventricular remodeling in patients with large acute myocardial infarction: the Delapril Remodeling after Acute Myocardial Infarction (DRAMI) trial

Background

In the large-scale trial, Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico-3 (GISSI-3), patients receiving the combination of lisinopril and glyceryl trinitrate benefited most from experimental therapy. Therefore, a multicenter, randomized, double-blind study, Delapril Remodeling After Acute Myocardial Infarction (DRAMI), was designed to assess (1) the possible additive beneficial effect on left ventricular remodeling of nitrates when combined with an angiotensin-converting enzyme inhibitor (ACEI), and (2) the tolerability of a new ACEI, delapril, in respect to lisinopril in patients with large myocardial infarction (MI).

Methods

A total of 177 patients were randomized to receive delapril plus isosorbide-5-mononitrate (IS5MN) placebo, delapril plus IS5MN, lisinopril plus IS5MN placebo, or lisinopril plus IS5MN starting within the first 36 hours after the onset of symptoms and continuing for 3 months.

Results

More than 80% of the patients showed extensive ST-segment changes and 36.7% had signs or symptoms of heart failure during the first 36 hours. Over 3 months, IS5MN reduced, by 76%, the increase in LVEDV (17.4 ± 5.0 mL placebo vs 4.2 ± 4.4 mL IS5MN, P = .0439), reversed the increase in LVESV (7.5 ± 3.9 mL placebo vs −5.5 ± 2.9 mL IS5MN, P = .0052), and increased the recovery of LVEF (1.9% ± 1.3% placebo vs 6.7% ± 1.2% IS5MN, P = .0119). Overall, 3-month mortality was 10.2%; the most frequent clinical events were new episodes of severe heart failure (18.1%), persistent hypotension (10.7%), and post-MI angina (18.1%), with no differences between treatment groups.

Conclusions

Administration for 3 months of IS5MN combined with an ACEI, both started within 36 hours from the onset of symptoms, was safe and effective in reducing LV dilation and dysfunction after MI. The 2 ACEIs, delapril and lisinopril, appeared to be equally well tolerated.     

Alcohol intake is not associated with subclinical coronary atherosclerosis

Background

The inverse relation between alcohol intake and clinical coronary artery disease (CAD) is well established, although the mechanisms remain speculative. We studied the relation between alcohol intake and subclinical CAD to assess the possible role of alcohol in atherogenesis.

Methods

We conducted a prospective study of 731 consecutive, consenting, active-duty US Army personnel (39 to 45 years of age) without known CAD who were undergoing a routine physical examination. Each participant was surveyed with the validated Block dietary questionnaire, which included detailed information on alcohol intake as wine, beer, or liquor. Subclinical CAD was determined by means of electron beam computed tomography to quantify coronary artery calcification (CAC).

Results

The mean age was 42 (±2); 83% were male, 71% were white, and 82% were college graduates. The prevalence of CAC was 18.6% (mean CAC score = 12 ± 69). Twenty-two percent drank alcohol daily, with an average of 2.4 drinks per day. Systolic blood pressure was correlated with number of drinks per day (r = 0.10, P = .025). Among drinkers, HDL was weakly correlated with daily alcohol consumption (r = 0.10, P = .025). There was no relation between the CAC score and the alcohol intake as measured by drinks per day (OR, 1.02; 95% CI, 0.64 to 1.63; 1.13, 0.59 to 2.15; 1.26, 0.69 to 2.59, for less than 1, 1 to 2, and more than 2 drinks per day, respectively). Stratified analyses based on type of alcohol and multivariate analyses indicated no independent relation between any type or quantity of alcohol intake and the presence or extent of coronary calcification.

Conclusions

Alcohol intake does not appear to be inversely related to subclinical CAC, implying that previous observations of a protective effect of alcohol on clinical CAD may involve factors related to plaque stability rather than atherogenesis.     

ST-segment deviation on the admission electrocardiogram, treatment strategy, and outcome in non-ST-elevation acute coronary syndromes : A substudy of the Invasive versus Conservative Treatment in Unstable coronary Syndromes (ICTUS) Trial

Background

We assessed the prognostic significance of the presence of cumulative (∑) ST-segment deviation on the admission electrocardiogram (ECG) in patients with non-ST-elevation acute coronary syndrome and an elevated troponin T randomized to a selective invasive (SI) or an early invasive treatment strategy.

Methods

A 12-lead ECG obtained at admission was available for analysis from 1163 patients. The presence and magnitude of ST-segment deviation was measured in each lead, and absolute ST-segment deviation was summed. The effect of treatment strategy was assessed for patients with or without ∑ ST-segment deviation of at least 1 mm.

Results

The incidence of death or myocardial infarction (MI) by 1 year in patients with ∑ ST-segment deviation of at least 1 mm was 18.0% compared with 11.1% in patients with ∑ ST-segment deviation of less than 1 mm (P = .001). Among patients with ∑ ST-segment deviation of at least 1 mm, the incidence of death or MI was 21.9% in the early invasive group compared with 14.2% in SI group (P < .01). However, we observed a significantly higher rate of MI after hospital discharge among patients with ∑ ST-segment deviation of at least 1 mm randomized to SI who did not undergo angiography compared with patients who underwent angiography before discharge (10.9% vs 2.4%, P = .003). In a forward logistic regression analysis, the presence of ST-segment deviation was an independent predictor for failure of medical therapy (coronary angiography within 30 days after randomization in the SI group) (odds ratio, 1.56; 95% confidence interval, 1.12-2.18; P = .009).

Conclusion

Patients with non-ST-elevation acute coronary syndrome and an elevated troponin T and ∑ ST-segment deviation of at least 1 mm are at increased risk of death or MI, more often fail on medical therapy, and more often experience a spontaneous MI after discharge when angiography was not performed during initial hospitalization.     

Impact of electrical neurostimulation on persistent ST elevation after successful reperfusion by primary percutaneous coronary intervention

Aims

To study the effect of electrical neurostimulation on the ST segment shift in patients with ST elevation myocardial infarction (STEMI) with residual ST elevation after primary percutaneous coronary intervention (PCI).

Methods

After primary PCI, 38 patients with STEMI were divided into 2 groups. Group 1 received 15 minutes of active neurostimulation after the baseline electrocardiogram (ECG); group 2 received 15 minutes of active neurostimulation after 15 minutes of nonactive neurostimulation.

Results

In group 1, ST elevation decreased with neurostimulation from 0.65 ± 0.56 to 0.55 ± 0.51 (P = .02) and to 0.50 ± 0.52 (P = .01) without electrical neurostimulation. In group 2, ST elevation changed without neurostimulation from 0.37 ± 0.32 to 0.33 ± 0.30 (P = NS) and to 0.28 ± 0.27 (P = .01) with electrical neurostimulation. In a posthoc analysis, 17 responders had higher ST elevation at the ECG before active electrical neurostimulation than 21 nonresponders (P = .001).

Conclusion

Electrical neurostimulation may result in significant additional reduction of ST elevation in STEMI after reperfusion treatment, in particular in patients with marked ST elevation on the first ECG after successful primary PCI.     

Hyponatremia in marathon runners due to inappropriate arginine vasopressin secretion

Purpose

Exercise-associated hyponatremia (EAH), as defined by a blood sodium concentration [Na⁺] less than 135 mmol/L, may lead to hypotonic encephalopathy with fatal cerebral edema. Understanding the pathogenetic role of antidiuresis may lead to improved strategies for prevention and treatment.

Methods

Normonatremic marathon runners were tested pre- and post-race for creatine kinase, interleukin-6, cortisol, prolactin, and arginine vasopressin. Similar testing also was carried out in runners with encephalopathy caused by EAH, including 2 cases with fatal cerebral edema.

Results

Normonatremic runners (n = 33; 2001) with a mean 3% decrease in body weight showed a 40-fold increase in interleukin-6 (66.6 ± 11.9 pg/mL from 1.6 ± 0.5 pg/mL, P = .001), which was significantly correlated with increases in creatine kinase (r = 0.88, P = <.0001), cortisol (r = 0.70, P = .0003), and prolactin (r = 0.67, P <.007), but not arginine vasopressin (r = 0.44, P = .07). Collapsed runners with EAH (n = 22; 2004) showed a mean blood urea nitrogen less than 15 mg/dL with measurable plasma levels of arginine vasopressin (>0.5 pg/mL) in 43% of cases. Two marathon runners with fatal cerebral edema additionally showed less than maximally dilute urines (>100 mmol/kg/H₂O) and urine [Na⁺] greater than 25 mEq/L.

Conclusions

Cases of EAH fulfill the essential diagnostic criteria for the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Runners with hypotonic encephalopathy at subsequent races were treated with intravenous hypertonic (3%) saline on the basis of this paradigm, which resulted in rapid clinical improvement without adverse effects. Release of muscle-derived interleukin-6 may play a role in the nonosmotic secretion of arginine vasopressin, thereby linking rhabdomyolysis to the pathogenesis of EAH.