Reduction of Left Ventricular Dilation Beyond the First Year After Anterior Myocardial Infarction.

BACKGROUND: Reduction of left ventricular (LV) dilation (RD) beyond the first year after ST-segment-elevation myocardial infarction (STEMI) is unknown. We investigated its potential occurrence in comparison with stationary (SD) and progressive (PD) dilation. METHODS AND RESULTS: Perfusion gated SPECT features at 1 and 3 years were evaluated in 168 3-year survivors of a first anterior STEMI. Comparisons were made among patients with RD (≥15% reduction of LV end-systolic volume [LVESV]), SD (<15% reduction or increase), and PD (≥15% increase). There were 35 patients with RD (21%), 84 with SD (50%), and 49 with PD (29%). At 1 year, ejection fraction, wall motion and perfusion scores, and LV volumes were similar. In RD patients, the fall in LVESV, nearly 22%, was apparent in those with frank (>51 mL; P < .001) or little/moderate LV dilation at 1 year (LVESV ≤51 mL; P = .002) and was associated with increased ejection fraction (P values .008 and .009, respectively). In the 3 groups, however, LVESV changes were unrelated to 1-year LV volumes, ejection fraction, or contractility score. CONCLUSIONS: At 3 years following anterior STEMI there is reduction of LV dilation in about 21% of patients associated with increases in ejection fraction in those with or without clearly dilated ventricles at 1year. These findings add to the complexity of LV remodeling and possibly suggest very late changes in infarct size.

Resting-State Functional Connectivity Magnetic Resonance Imaging and Outcome After Acute Stroke.

Background and Purpose- Physiological effects of stroke are best assessed over entire brain networks rather than just focally at the site of structural damage. Resting-state functional magnetic resonance imaging can map functional-anatomic networks by analyzing spontaneously correlated low-frequency activity fluctuations across the brain, but its potential usefulness in predicting functional outcome after acute stroke remains unknown. We assessed the ability of resting-state functional magnetic resonance imaging to predict functional outcome after acute stroke. Methods- We scanned 37 consecutive reperfused stroke patients (age, 69±14 years; 14 females; 3-day National Institutes of Health Stroke Scale score, 6±5) on day 3 after symptom onset. After imaging preprocessing, we used a whole-brain mask to calculate the correlation coefficient matrices for every paired region using the Harvard-Oxford probabilistic atlas. To evaluate functional outcome, we applied the modified Rankin Scale at 90 days. We used region of interest analyses to explore the functional connectivity between regions and graph-computation analysis to detect differences in functional connectivity between patients with good functional outcome (modified Rankin Scale score ≤2) and those with poor outcome (modified Rankin Scale score >2). Results- Patients with good outcome had greater functional connectivity than patients with poor outcome. Although 3-day National Institutes of Health Stroke Scale score was the most accurate independent predictor of 90-day modified Rankin Scale (84.2%), adding functional connectivity increased accuracy to 94.7%. Preserved bilateral interhemispheric connectivity between the anterior inferior temporal gyrus and superior frontal gyrus and decreased connectivity between the caudate and anterior inferior temporal gyrus in the left hemisphere had the greatest impact in favoring good prognosis. Conclusions- These data suggest that information about functional connectivity from resting-state functional magnetic resonance imaging may help predict 90-day stroke outcome.

Diffusion tensor imaging as a prognostic biomarker for motor recovery and rehabilitation after stroke.

PURPOSE: Despite improved acute treatment and new tools to facilitate recovery, most patients have motor deficits after stroke, often causing disability. However, motor impairment varies considerably among patients, and recovery in the acute/subacute phase is difficult to predict using clinical measures alone, particularly in severely impaired patients. Accurate early prediction of recovery would help rationalize rehabilitation goals and improve the design of trials testing strategies to facilitate recovery. METHODS: We review the role of diffusion tensor imaging (DTI) in predicting motor recovery after stroke, in monitoring treatment response, and in evaluating white matter remodeling. We critically appraise DTI studies and discuss their limitations, and we explore directions for future study. RESULTS: Growing evidence suggests that combining clinical scores with information about corticospinal tract (CST) integrity can improve predictions about motor outcome. The extent of CST damage on DTI and/or the overlap between the CST and a lesion are key prognostic factor that determines motor performance and outcome. Three main strategies to quantify stroke-related CST damage have been proposed: (i) measuring FA distal to the stroke area, (ii) measuring the number of fibers that go through the stroke with tractography, and (iii) measuring the overlap between the stroke and a CST map derived from healthy age- and gender-matched controls. CONCLUSION: Recovery of motor function probably involves remodeling of the CST proper and/or a greater reliance on alternative motor tracts through spontaneous and treatment-induced plasticity. DTI-metrics represent promising clinical biomarkers to predict motor recovery and to monitor and predict the response to neurorehabilitative interventions.

Decreased corticospinal tract fractional anisotropy predicts long-term motor outcome after stroke.

BACKGROUND AND PURPOSE: Nearly 50% of patients have residual motor deficits after stroke, and long-term motor outcome is difficult to predict. We assessed the predictive value of axonal damage to the corticospinal tract indexed by diffusion tensor imaging fractional anisotropy for long-term motor outcome. METHODS: Consecutive patients with middle cerebral artery stroke underwent multimodal MRI, including diffusion tensor imaging ≤12 hours, 3 days, and 30 days after onset. Clinical severity, infarct volume, location of corticospinal tract damage on diffusion tensor tractography, and ratios of fractional anisotropy (rFA) between affected and unaffected sides of the corticospinal tract at the pons were evaluated. Severity of motor deficit at 2 years was categorized using the Motricity Index as no deficit (Motricity Index, 100), slight-moderate deficit (Motricity Index, 99-50), or severe deficit (Motricity Index, <50). RESULTS: We evaluated 70 patients (28 women; 72±12 years). rFA values at day 30 correlated with the degree of motor deficit at 2 years (P<0.001). rFA at day 30 was the only independent predictor of long-term motor outcome (odds ratio, 1.60; 95% confidence interval, 1.26-2.03; P<0.001). The sensitivity, specificity, and positive and negative predictive values of the cutoffs rFA<0.982 for predicting slight-moderate deficit and rFA<0.689 for severe deficit were 94.4%, 84.6%, 73.9%, and 97.1%, respectively, and 100%, 83.3%, 81.3%, and 100%, respectively. CONCLUSIONS: rFA at day 30 is an independent predictor of long-term motor outcome after stroke.

Acute myocardial infarction: estimation of at-risk and salvaged myocardium at myocardial perfusion SPECT 1 month after infarction.

PURPOSE: To estimate at-risk and salvaged myocardium by using gated single photon emission computed tomography (SPECT) myocardial perfusion imaging after acute myocardial infarction (AMI). MATERIALS AND METHODS: The study was approved by the hospital's Ethical Committee on Clinical Trials (trial register number, PR(HG)36/2000), and all patients gave informed consent. Forty patients (mean age, 61.78 years; eight women) with a first AMI underwent two gated SPECT examinations--one before percutaneous coronary intervention (PCI) and one 4-5 weeks after PCI. Myocardium at risk was estimated by assessing the perfusion defect at the first gated SPECT examination, and salvaged myocardium was estimated by assessing the risk area minus necrosis at the second examination. Myocardium at risk was estimated by determining the discordance between the areas of left ventricular (LV) wall motion and perfusion at the second examination. Concordance between tests was analyzed by means of linear regression analysis, the Pearson correlation, the intraclass correlation coefficient, and Bland-Altman analysis. RESULTS: An improvement in perfusion, wall motion, wall thickening, and LV ejection fraction (P < .001) was observed at 1 month. At 1 month, the area with abnormal wall motion was greater than the area of altered perfusion (35.47 vs 23.1 cm(2); P = .007). The extent of myocardium at risk estimated from this discordance correlated well with myocardium at risk measured at the first gated SPECT examination and with salvaged myocardium between both studies (Pearson correlation: 0.78 and 0.6, respectively). Concordance for correct classification of patients with salvaged myocardium of 50% or greater was 83% (κ = 0.65). CONCLUSION: Myocardial perfusion gated SPECT performed 1 month after early PCI in a first AMI provides potentially useful information on at-risk and salvaged myocardium. SUPPLEMENTAL MATERIAL: http://radiology.rsna.org/lookup/suppl/doi:10.1148/radiol.13122324/-/DC1.

Hospital outcome of moderate to severe pericardial effusion complicating ST-elevation acute myocardial infarction.

BACKGROUND: Hospital prognosis of moderate to severe pericardial effusion (MPE; ≥10 mm) in ST-elevation myocardial infarction is largely unknown. METHODS AND RESULTS: Data from 446 ST-elevation myocardial infarction patients, 228 with MPE-88 with cardiac tamponade (CT) and electromechanical dissociation (EMD), 44 with CT without EMD (w/oEMD), and 96 without initial CT-and 218 with small PE (5 to 9 mm), were compared. Patients with MPE without initial CT were also compared with 96 patients without PE. CT patients showed larger PE (P<0.001) than those without initial CT; 85% of those with CT+EMD and 86% with CTw/oEMD were treated with pericardiocentesis and 10% and 21% were treated with a surgical repair, respectively. Among MPE patients, 30-day mortality was 43% and was higher in those with CT+EMD (operated, 89%; and nonoperated, 85%) than in those with CTw/oEMD (22% and 11%, respectively; P<0.001) and those without initial CT (17%; P<0.001). It was also higher than in patients with small PE (10%; P<0.001) or those without PE (6%; P=0.001). Death was attributable to cardiac rupture in 83% of patients with CT+EMD, 7% with CTw/oEMD, and 8% with MPE without initial CT and occurred late (≥7 days) in 14%, 67%, and 100%, respectively. CONCLUSIONS: MPE carries an increased mortality that is highest in patients with CT+EMD. In those with CTw/oEMD, however, mortality is considerably low after pericardiocentesis, and subsequent management may be individualized because a conservative approach is often successful. Importantly, MPE patients without initial CT are not free from late rupture and deserve further investigation.

Prothrombotic profile in patients with vasospastic or non vasospastic angina and non significant coronary stenosis.

BACKGROUND: Patients with vasospastic (VA) or non vasospastic angina (NVA) without significant coronary stenosis have a reduced risk of infarction but is unclear whether or not this may be attributable to a lack of prothrombotic profile - similar to that present in patients with stable coronary artery disease (CAD). METHODS: Plasma levels of von Willebrand factor, total and free tissue factor pathway inhibitor, plasminogen activator inhibitor-1, and fibrinogen were analyzed in 15 patients with stable VA and 23 with NVA, all with vasoconstrictive response to acetylcholine although with different severity. Results were compared with those of 20 age-matched controls and 10 patients with CAD. RESULTS: Plasma levels of von Willebrand factor in patients with VA or NVA were higher than in controls (207 ± 62 and 203 ± 69% vs 121 ± 38%, p < 0.001) and tended to be lower than in CAD patients (264 ± 65, p = 0.145). They also presented higher total tissue factor pathway inhibitor (123 ± 18 and 111 ± 25 vs 88 ± 14, ng/ml p < 0.001) and plasminogen activator inhibitor-1 levels than controls (51 ± 30 and 52 ± 31% vs 19 ± 9 ng/ml, p < 0.001) and similar to CAD patients (134 ± 23 and 62 ± 31, respectively, ns). Moreover, free tissue factor pathway inhibitor plasma levels were lower than controls (18 ± 5 and 17 ± 5 vs 23 ± 8 ng/ml, p = 0.002) and similar to CAD patients (14 ± 5, ns). Despite this prothrombotic condition none of VA or NVA patients presented a myocardial infarction during a 9 year follow-up, an observation also reported in larger series. CONCLUSIONS: During a stable phase of their disease, patients with VA or NVA present a prothrombotic profile that might eventually contribute to occurrence of myocardial infarction. The rarity of these events, however, may suggests that ill defined factors would protect these patients from coronary plaque rupture/fissure.

Changes in hospital mortality rates in 425 patients with acute ST-elevation myocardial infarction and cardiac rupture over a 30-year period.

BACKGROUND: Possible changes in the incidence and outcome of cardiac rupture in patients with ST-elevation myocardial infarction over a long period of time have not been investigated. METHODS AND RESULTS: The incidence of cardiac rupture in ST-elevation myocardial infarction patients and its mortality rate were investigated during a 30-year period divided into 5 intervals (1977 to 1982, 1983 to 1988, 1989 to 1994, 1995 to 2000, and 2001 to 2006). Of a total of 6678 consecutive patients, 425 experienced a free wall rupture (280 with cardiac tamponade: 227 with electromechanical dissociation and 53 with hypotension) or a septal rupture (145). After the exclusion of referrals from other centers (n=44), the incidence of definite cardiac rupture (septal rupture, anatomic evidence of free wall rupture, or electromechanical dissociation) declined progressively (6.2% in 1977 to 1982 to 3.2% in 2001 to 2006; P<0.001) in parallel with a progressive use of reperfusion therapy (0% to 75.1%; P<0.001). In addition, among patients with cardiac rupture, there was a progressive fall in the rate of death (94% to 75%; P<0.001) despite a trend toward increasing age (66+/-8 to 75+/-8 years; P<0.054) in conjunction with better control of systolic blood pressure at 24 hours (130+/-24 versus 110+/-18 mm Hg; P<0.001); an increased use of reperfusion therapy (0% to 59%; P<0.001), beta-blockers (0% to 45%; P<0.001), angiotensin-converting enzyme inhibitors (0% to 38%; P<0.001), and aspirin (0% to 96%; P<0.001); and a lower use of heparin (99% to 67%; P<0.001). CONCLUSIONS: The decline in the incidence in cardiac rupture and its rate of death over the last 30 years appears to be associated with the increasing use of reperfusion strategies and adjunct medical therapy.

High incidence of TIMI flow 0 to I in patients with ST-elevation myocardial infarction without electrocardiographic lytic criteria.

BACKGROUND: Most patients with ST-elevation myocardial infarction fulfilling ST-segment elevation (STE) lytic criteria present an occluded culprit artery but the occlusion rate in those with minimal STE (minSTE) not fulfilling lytic criteria is unknown. METHODS: In 63 patients with minSTE (mean STE:1.2 +/- 0.6 mm) and 149 with lytic STE criteria (lyticSTE, 4.8 +/- 3.1 mm), an emergency coronary angiography was performed, serial creatine kinase-MB was determined, and ejection fraction was measured by 2-dimensional echocardiography. RESULTS: The 2 groups showed similar time from pain onset to electrocardiogram (minSTE 196 +/- 199 vs lyticSTE, 176 +/- 172 min, P = .444), and although time to catheterization was longer in patients with minSTE (426 +/- 314 vs 253 +/- 239 min, P < .001), the rate of TIMI flow 0 to I (88% vs 81%, P = .21) was similar and percutaneous coronary intervention was performed in >80% of patients from the 2 groups. Moreover, patients with minSTE had higher rate of collateral circulation (27% vs 13%, P = .013), lower rate of Q waves (44% vs 60%, P = .041), lower creatine kinase-MB (202 +/- 150 vs 335 +/- 280, microg/L, P < .001), higher ejection fraction (54% +/- 9% vs 49% +/- 12%, P = .004), and lower mortality (0% vs 7.4%, P = .036). CONCLUSIONS: ST-elevation myocardial infarction patients with minSTE present a high prevalence of TIMI flow 0 to I similar to those meeting lyticSTE suggesting an identical underlying mechanism and the potential to benefit from primary angioplasty.

[III Catalan registry of ST elevation acute myocardial infarction. Comparison with former Catalan registries I and II from Catalonia, Spain]. / Resultados del III registro IAM CAT de pacientes con infarto de miocardio con elevación del segmento ST en Cataluña. Comparación con los registros IAM CAT I y II.

BACKGROUND AND OBJECTIVE: To analyze the use of reperfusion therapy in patients with ST elevation myocardial infarction (STEMI) in Catalonia in a registry performed in 2006 (IAM CAT III) and its comparison with 2 previous registries PATIENTS AND METHODS: Frequency of reperfusion therapy and time intervals between symptom onset - reperfusion therapy were the principal variables investigated. The IAM CAT I (June-December 2000) included 1,450 patients, the IAM CAT II (October 2002-April 2003) 1,386, and the IAM CAT III (October-December 2006) 367. RESULTS: The proportion of patients treated with reperfusion increased progressively (72%, 79% and 81%) as the use of primary angioplasty (5%, 10% and 33%). In the III registry the transfer system most frequently used was the SEM/061 (17%, 32% and 47%, respectively) but the time interval symptom onset-first contact with the medical system did not improve (II, 90 vs III, 105 min), the interval symptom onset-thrombolytic therapy did hardly change (178, 165 and 177 min) and the interval hospital arrival-trombolysis (needle-door) tended to improve (59, 42 and 42 min). Thirty day mortality in STEMI patients declined progressively through the 3 registries (12.1, 10.6 and 7.4%, p=0.012). CONCLUSIONS: The proportion of STEMI patients treated with reperfusion has improved but the interval to its application has not been shortened. To improve the latter it is mandatory an earlier contact with the medical system, a shortening of the intervals door-needle and door-balloon through better coordination between the 061, the sanitary personnel and the hospital administration, and to consider the subject as a real sanitary priority.

Comparison of distinctive clinical and cardiac magnetic resonance features between ST elevation myocardial infarction patients with incomplete myocardial rupture and those with moderate to severe pericardial effusion.

BACKGROUND: Whether patients with incomplete myocardial rupture (IMR) present distinctive clinical and cardiac magnetic resonance features from those with moderate-severe pericardial effusion (⩾10 mm (PE)) remains unknown. METHODS: We compared the clinical, angiographic and cardiac magnetic resonance characteristics of nine patients with IMR (diagnosed angiographically and/or by cardiac magnetic resonance) with 29 with PE, and also with 38 without IMR or PE with evidence of transmural necrosis (reference group) matched for age, gender and year of admission. RESULTS: Patients with IMR were younger than those with PE (p<0.001) but the two groups shared a higher rate of admission delay (78% and 41%) than those without IMR/PE (5%, p<0.001) and lower frequency of reperfusion therapy (44%, 55% and 100%, respectively, p<0.001). Thirteen patients with PE (45%) but only one IMR (11%) presented recurrent chest pain. IMR patients tended to present smaller infarct size at cardiac magnetic resonance (p=0.153 and 0.036) and number of segments with ⩾75% necrosis than PE patients and those without IMR/PE (p=0.098 and 0.029, respectively). Ten PE patients presented cardiac tamponade (35%). A control 2D-echocardiogram performed within two years in 71 patients (93%) documented a pseudoaneurysm in one PE and in one IMR patient. CONCLUSIONS: IMR is generally silent and occurs in younger patients with smaller infarct size than those with PE although both present late and are often untreated with reperfusion therapy. These findings may warrant imaging assessment in ST elevation myocardial infarction patients with delayed admission, particularly in absence of reperfusion, to rule out an IMR.

Reverse, stationary and progressive left ventricular dilatation in dilated and nondilated ventricles on admission following first anterior STEMI.

BACKGROUND: The relationship between admission left ventricular (LV) volumes, regional contractility and persistent ST elevation in first anterior ST elevation myocardial infarction (STEMI) with evolution of LV volumes at 12 months remains inconclusive. Thus possible differences among patients with reverse dilatation (RD), stationary dilatation (SD) or progressive dilatation (PD) at 12 months based on left ventricle end-systolic volume (LVESV) index changes were investigated. PATIENTS AND METHODS: ECG and echocardiographic features of 394 1-year survivors of anterior STEMI were analyzed at admission, 6 and 12 months in those with RD (≥15% reduction of LVESV index, at 12 months n=141), SD (<15% reduction or increase, n=123) or PD (≥15% increase, n=130). Long-term outcome was also evaluated. RESULTS: Admission LVESV values in tertiles and incidence of moderate-severe mitral regurgitation were similar in three groups. In patients with RD, LVESV decreased at 6 months (P<0.001) and further at 12 months (P=0.003), whereas in PD, it increased at 6 months (P<0.001) and further at 12 months (P=0.016). Contractility score in PD was higher on admission (P=0.050) than in the other groups, but it involved the same segments. At 12 months, it improved in each of the six most affected in RD (P<0.001) and SD (P=0.025-0.001) but not in PD group (P=0.452-1.00). Persistent ST elevation at 24 h and peak troponin I were the only independent predictors for RD (odds ratio: 0.900, 95% confidence interval: 0.840-0.905, P=0.003; 0.996, 0.986-0.994, P<0.001) and PD (1.143, 1.001-1.304, P=0.048; 1.004, 1.002-1.006, P<0.001), respectively. During an 8-year follow-up, 77 (19.5%) patients died and although the total mortality was comparable in the three groups, cardiac death or hospitalization for heart failure was higher in the PD (16/130, 14%) than in the other two groups (14/250, 5.6%, P=0.014). CONCLUSION: Admission normal or enlarged LV volumes may evolve towards RD, SD or PD at 12 months following first anterior STEMI mainly depending in part on infarct size. Importantly, relevant changes occur at not only 6 months but also between 6 and 12 months.

Area at risk and collateral circulation in a first acute myocardial infarction with occluded culprit artery. STEMI vs non-STEMI patients.

BACKGROUND: It is unclear why among patients with first acute myocardial infarction and an occluded culprit artery only some present ST segment elevation. In fact, there is no study that compares the angiographic area at risk and the collateral circulation in first NSTEMI vs STEMI patients. METHODS AND RESULTS: 205 patients admitted for myocardial infarction with occluded culprit artery were included, 132 STEMI and 73 NSTEMI. Demographic data, the area at risk determined by the BARI score and collateral supply by the Rentrop score from the 2 groups were compared. NSTEMI patients showed lower peak Tn I than STEMI in the overall group but also in the 3 subsets with different culprit arteries (p < .001). They also presented a higher rate of left circumflex coronary artery (CFX) as culprit artery (52% vs 14%, p < .001), smaller BARI score area of the culprit artery (5.4 vs 7.6, p < .001), and higher frequency of well-developed collaterals (Rentrop score ≥ 2, 1.82 vs 0.41, p < .001). The latter was also higher in each of the 3 different culprit arteries (p = .002-<0.001) Among 38 NSTEMI patients with CFX occlusion, 20 with ≥1 mm ST depression in V2 to V4 (possible posterior infarction) showed a similar Rentrop score than the 18 with other ECG changes but lower Tn I peak (p = .012). CONCLUSIONS: In first acute myocardial infarction with an occluded culprit artery NSTEMI patients - including those with possible posterior infarction - present smaller infarct size and higher collateral blood supply than STEMI patients in each of the 3 main culprit arteries.

Effect of clinical variables on the correlation between amount of ST elevation and myocardial scintigraphic perfusion defect during coronary occlusion.

PURPOSE: We investigated if the correlation between the amount of ST elevation (STE) and myocardial ischemia could be altered by variables such as hypertension or body mass index (BMI). METHODS: A 12-lead electrocardiogram and a technetium-99m tetrofosmin injection were performed during balloon coronary occlusion in 34 patients with single-vessel disease. RESULTS: The sum of STE correlated with scintigraphic extent of ischemia (r = 0.441; P = .009), but this correlation improved significantly in men and patients with BMI of 28 kg/m2 or less and was highest in nonhypertensive patients (r = 0.763; P < .001). In contrast, it was poor in women and patients with BMI greater than 28 kg/m2 or arterial hypertension, being lowest in the latter subset (r = 0.110; P = .664). Moreover, 8 (80%) of 10 patients with extensive hypoperfusion but with low SigmaSTE (< or =20 mm) were hypertensive. CONCLUSIONS: If confirmed by larger studies, electrocardiographic underestimation of transmural ischemia during coronary occlusion in patients with hypertension or increased BMI may lead to adjustments in STE criteria for reperfusion therapy.

Comparison of clinical and angiographic features and longterm follow-up events between patients with variant angina and patients with ST elevation myocardial infarction.

We investigated to what extent patients with variant angina and significant coronary stenosis (>or=70%) present a clinical and angiographic profile similar to patients with ST elevation myocardial infarction. Thus, the clinical and angiographic features as well as follow-up events of 200 patients were prospectively analyzed and were compared with those of 422 patients with a first ST elevation myocardial infarction survivors of the early phase (3 days) and those of 70 patients with variant angina and non significant stenosis. Age and incidence of smoking, systemic hypertension, diabetes and maximum ST elevation were similar in the 2 groups. Furthermore, among patients with significant coronary stenosis, stenosis severity and the proportion of eccentric lesions were also comparable. Incidence of recent-within 30 days prior to admission-angina at rest was higher in variant angina patients with significant stenosis (67% vs. 27%, p<0.001) than in those with myocardial infarction but long standing angina at rest (>30 days) was low and comparable in these 2 groups (15% vs. 11%, ns). Also, in a 5-year follow-up most patients from these 2 groups were free from angina at rest (86% vs. 84%) which in variant angina patients was largely attributable to a high revascularization rate (72%). Moreover, the rate of myocardial infarction/cardiac death (20% vs. 19%) was also similar. Patients with variant angina and non-significant stenosis, however, had longer antecedent angina, more frequent follow-up angina and a lower incidence of cardiac events than the other 2 groups. Thus, these findings suggest that patients with variant angina and significant coronary stenosis generally behave as an acute coronary syndrome-likely associated with an acutely complicated plaque-rather than as recurrent vasospastic angina, and should be managed accordingly.

Predischarge low-dose dobutamine test and prediction of left ventricular function at 1 year in patients with a first anterior myocardial infarction.

BACKGROUND: It is unclear whether spontaneous improvement in contractility following acute myocardial infarction (AMI) is related to severity of predischarge systolic dysfunction and can be predicted by isotopic ventriculography with a low-dose dobutamine test (DBT). HYPOTHESIS: Spontaneous improvement in contractility would be similar in patients with more preserved and those with depressed ventricular function, and a DBT test could predict it. METHODS: Left ventricular ejection fraction (LVEF), regional contractility score (RCS), and left ventricular end-diastolic volume index (EDVI) at predischarge, during DBT, and at 1 year were analyzed in 43 patients with a first anterior ST-elevation AMI. RESULTS: Changes produced by DBT in patients with LVEF < 40%, RCS > or = 3, or EDVI > or = 70 ml/m2 were smaller than in those observed at 1 year (LVEF: 30 +/- 5-35 +/- 7%, p < 0.001, vs. 39 +/- 10%, p = 0.005; RCS: 4.9 +/- 1.4-4.6 +/- 2.0, NS, vs. 3.4 +/- 2.0, p < 0.02; EDVI: 92 +/- 14-86 +/- 22, NS, vs. 78 +/- 23 ml/m2, p < 0.03). In contrast, in patients with EF > or = 40%, RCS < 3 or EDVI < 70 ml/m2, changes with DBT tended to be greater than those observed at 1 year (LVEF: 52 +/- 8-57 +/- 11%, p < 0.004 vs. 55 +/- 11%, p < 0.04); RCS: 1.1 +/- 0.9-0.8 +/- 0.8, NS, vs. 1.1 +/- 1.1, NS; and EDVI: 51 +/- 9-47 +/- 11, p < 0.005, vs. 54 +/- 13 ml/m2, NS). CONCLUSIONS: Among patients with a first anterior AMI, spontaneous improvement in contractility at 1 year was greatest in those with a more depressed ventricular function or a dilated ventricle, but its magnitude was underestimated by a predischarge DBT test.

Hospital and 4-Year Mortality Predictors in Patients With Acute Pulmonary Edema With and Without Coronary Artery Disease.

BACKGROUND: Long-term prognosis of acute pulmonary edema (APE) remains ill defined. METHODS AND RESULTS: We evaluated demographic, echocardiographic, and angiographic data of 806 consecutive patients with APE with (CAD) and without coronary artery disease (non-CAD) admitted from 2000 to 2010. Differences between hospital and long-term mortality and its predictors were also assessed. CAD patients (n=638) were older and had higher incidence of diabetes and peripheral vascular disease than non-CAD (n=168), and lower ejection fraction. Hospital mortality was similar in both groups (26.5% vs 31.5%; P=0.169) but APE recurrence was higher in CAD patients (17.3% vs 6.5%; P<0.001). Age, admission systolic blood pressure, recurrence of APE, and need for inotropics or endotracheal intubation were the main independent predictors of hospital mortality. In contrast, overall mortality (70.0% vs 57.1%; P=0.002) and readmission for nonfatal heart failure after a 45-month follow-up (10-140; 17.3% vs 7.6%; P=0.009) were higher in CAD than in non-CAD patients. Age, peripheral vascular disease, and peak creatine kinase MB during index hospitalization, but not ejection fraction, were the main independent predictors of overall mortality, whereas coronary revascularization or valvular surgery were protective. These interventions were mostly performed during hospitalization index (294 of 307; 96%) and not intervened patients showed a higher risk profile. CONCLUSIONS: Long-term mortality in APE is high and higher in CAD than in non-CAD patients. Considering the different in-hospital and long-term mortality predictors herein described, which do not necessarily involve systolic function, it is conceivable that a more aggressive interventional program might improve survival in high-risk patients.

Plasma bilirubin values on admission and ventricular remodeling after a first anterior ST-segment elevation acute myocardial infarction.

INTRODUCTION: Bilirubin may elicit cardiovascular protection and heme oxygenase-1 overexpression attenuated post-infarction ventricular remodeling in experimental animals, but the association between bilirubin levels and post-infarction remodeling is unknown. MATERIALS AND METHODS: In 145 patients with a first anterior ST-segment elevation acute myocardial infarction (STEMI), we assessed whether plasma bilirubin on admission predicted adverse remodeling (left ventricular end-diastolic volume [LVEDV] increase ≥20% between discharge and 6 months, estimated by magnetic resonance imaging). RESULTS: Patients' baseline characteristics and management were comparable among bilirubin tertiles. LVEDV increased at 6 months (P < 0.001) with respect to the initial exam, but the magnitude of this increase was similar across increasing bilirubin tertiles (10.8 [30.2], 10.1 [22.9], and 12.7 [24.3]%, P = 0.500). Median (25-75 percentile) bilirubin values in patients with and without adverse remodeling were 0.75 (0.60-0.93) and 0.73 (0.60-0.92) mg/dL (P = 0.693). Absence of final TIMI flow grade 3 (odds ratio 3.92, 95% CI 1.12-13.66) and a history of hypertension (2.04, 0.93-4.50), but not admission bilirubin, were independently associated with adverse remodeling. Bilirubin also did not predict the increase in ejection fraction at 6 months. CONCLUSIONS: Admission bilirubin values are not related to LVEDV or ejection fraction progression after a first anterior STEMI and do not predict adverse ventricular remodeling. Key messages Bilirubin levels are inversely related to cardiovascular disease, and overexpression of heme oxygenase-1 (the enzyme that determines bilirubin production) has prevented post-infarction ventricular remodeling in experimental animals, but the association between bilirubin levels and the progression of ventricular volumes and function in patients with acute myocardial infarction remained unexplored. In this cohort of patients with a first acute anterior ST-segment elevation myocardial infarction receiving contemporary management, bilirubin levels on admission were not predictive of the changes in left ventricular volumes or ejection fraction at 6 months measured by serial cardiac magnetic resonance imaging. The data are contrary to a significant protective effect of bilirubin against post-infarction ventricular remodeling.

Acute Arterial Hypertension in Acute Pulmonary Edema: Mostly a Trigger or an Associated Phenomenon?

BACKGROUND: The role of acute arterial hypertension in acute pulmonary edema (APE) as an associated or triggering phenomenon has been poorly investigated and is relevant to patient management. METHODS: This was a prospective observational study of clinical, electrocardiographic, and echocardiographic characteristics of patients with APE. Potential triggers, including acute coronary syndrome (ACS), rapid atrial fibrillation (AF) (≥ 120 bpm in AF), fever > 38°C or volume overload, isolated acute hypertension (systolic blood pressure ≥ 170 mm Hg), and unknown factors were investigated. RESULTS: There were 742 patients, 578 with coronary artery disease (78%), 116 with valvular heart disease or cardiomyopathy (16%), and 47 without identifiable heart disease (6%). ACS was present in 482 (65%) patients (silent in 154 of them), AF was present in 76 (10%) patients, fever/volume overload was present in 62 (8%) patients, acute hypertension was present in 50 (7%) patients, and no apparent trigger was seen in 72 (10%) patients. Admission hypertension occurred in 260 patients (35%): 155 (60%) with ACS (silent in 49 [32%]), 36 (14%) with AF, 19 (7%) with fever/volume overload, and 59 (19%) as an isolated trigger. Similar results were obtained when analyzing patients using coronary angiography (467 patients [63%]). Acute hypertension was present more frequently in patients with severe hypoventilation (arterial Pco2 > 60 mm Hg) than in those without (57% vs 29%; P < 0.001) and in those without moderate-severe mitral regurgitation than in those with (51% vs 30%; P < 0.001). CONCLUSIONS: In patients with APE, with or without ACS, acute hypertension is often present but mainly as an associated/reactive phenomenon and seems favoured by severe hypoventilation. Silent myocardial ischemia/necrosis deserves systematic investigation because it is not rare that it may be the underlying cause of APE.

Plasma B-type natriuretic peptide levels are poorly related to the occurrence of ischemia or ventricular arrhythmias during symptom-limited exercise in low-risk patients.

INTRODUCTION: The usefulness of B-type natriuretic peptide (BNP) as a marker of ischemia is controversial. BNP levels have predicted arrhythmias in various settings, but it is unknown whether they are related to exercise-induced ischemic ventricular arrhythmias. MATERIAL AND METHODS: We analyzed in 63 patients (64 ±14 years, 65% male, 62% with known coronary disease) undergoing exercise stress single-photon emission computed tomography (SPECT) the association between plasma BNP values (before and 15 min after exercise) and the occurrence of ischemia or ventricular arrhythmias during the test. RESULTS: Exercise test (8.1 ±2.7 min, 7.4 ±8.1 metabolic equivalents, 82 ±12% of maximal predicted heart rate) induced reversible perfusion defects in 23 (36%) patients. Eight (13%) patients presented significant arrhythmias (≥ 7 ventricular premature complexes/min, couplets, or non-sustained ventricular tachycardia during exercise or in the first minute of recovery). Median baseline BNP levels were 17.5 (12.4-66.4) pg/ml in patients developing scintigraphic ischemia and 45.6 (13.2-107.4) pg/ml in those without ischemia (p = 0.137). The BNP levels increased after exercise (34.4 (15.3-65.4)% increment over baseline, p < 0.001), but the magnitude of this increase was not related to SPECT positivity (35.7 (18.8-65.4)% vs. 27.9 (5.6-64.0)% in patients with and without ischemia, respectively, p = 0.304). No significant association was found between BNP values (at baseline or their change during the test) and ventricular arrhythmias. CONCLUSIONS: Plasma BNP values - at baseline or after exercise - were not associated with myocardial ischemia or with ventricular arrhythmia during exercise SPECT. These results highlight the limited usefulness of this biomarker to assess acute ischemia.