QT dispersion within the first 6 months after an acute myocardial infarction: relationship with systolic function, left ventricular volumes, infarct related artery status and clinical outcome.

INTRODUCTION: We analysed QT dispersion within the first 6 months postinfarction, its relationship with the main established risk stratifiers and its clinical value. METHODS AND RESULTS: In 55 patients with a first Q-wave myocardial infarction the 12-lead electrocardiogram was scanned and digitised for analysis of QT dispersion (QT maximum-QT minimum) at first day (72 [61-96] ms), first week (69 [47-90] ms), first month (67 [46-88] ms) and sixth month (47 [40-74] ms; P<0.0001 vs. first day). Cardiac catheterization was performed at first week and at sixth month; QT dispersion was not related to ejection fraction, left ventricular volumes, infarct related artery status or contractile reserve (improvement of the infarcted area with low-dose dobutamine); no relation was found between QT dispersion decrease from first week to sixth month with regional systolic function improvement. Finally, during a mean follow-up period of 35+/-22 months QT dispersion was not independently related to clinical events. CONCLUSION: QT dispersion decreases progressively during the first months after myocardial infarction. These changes should be taken into account to define cut-off values of clinical interest in this phase. This variable does not seem related to the classic prognosis predictors. In a nonselected postinfarction population it has a low clinical value.

[Determinants of contractile reserve in the infarction area. A quantitative study using dobutamine in contrast left ventriculography]. / Determinantes de la reserva contráctil en la zona del infarto. Estudio cuantitativo mediante ventriculografía de contraste con dobutamina.

AIM: The aim of this study was to relate the contractile reserve in infarction segments to the dysfunction at rest and to the residual coronary stenosis. METHODS: The study group consisted of 95 patients with a first myocardial infarction. Contrast left ventricular at baseline and after dobutamine infusion at 7.5 microg/kg/min and coronary angiograms were performed. The centerline method was used to quantify the extent of dysfunction (percentage of chords with dysfunction in the territory of the infarction artery) and its maximum severity (maximum units of standard deviation [SD] below the normal wall motion reference). Reduction of dysfunction extent with dobutamine was measured. RESULTS: On increasing baseline dysfunction severity, both the magnitude of the response to dobutamine ( 2 SD 3 SD 4 SD +/- 5 SD [n = 15] = 9+/-13%, > 5 SD [n = 13] = 3+/-4%, p = 0,0001), and the number of patients with a significant (> or =15%) positive response ( 2 SD 3 SD 4 SD 5 SD = 0%, p<0,0001) decreased. There were no differences in dobutamine improvement among the subgroups with (n = 84) or without (n = 11) significant stenosis in the infarction artery (18+/-15 vs. 16 +/-18%), or between the subgroups with a patent (n = 76, 18+/-19%) or occluded (n = 19, 11+/-11%) artery. CONCLUSIONS: Dobutamine response is related to dysfunction severity in the infarction area: when the severity is 5 (high negative response prevalence), dobutamine testing does not seem indicate. The existence of residual coronary stenosis does not attenuate contractile reserve at low dobutamine doses.

Wall motion of noninfarcted myocardium. Relationship to regional and global systolic function and to early and late left ventricular dilation.

We studied the wall motion of the noninfarcted area and its role in left ventricular remodeling. The study group consisted of 43 patients with a first Q-wave acute myocardial infarction and single-vessel disease. Cardiac catheterization was performed at the first week, and was repeated six months later. Left ventricular volumes, wall motion at the infarcted and noninfarcted area, ejection fraction and infarction-related artery status were quantified. Hyperkinesia was only found at the first week in 22% of cases, and at the sixth month in 26% of cases. Wall motion at the noninfarcted area correlated with wall motion at the infarcted area (one week: r=0.53 p<0.0001; six months: r=0.52 p=0.01), ejection fraction (one week: r=0.69 p<0.0001; six months: r=0.56 p=0.006), end-diastolic volume (one week: r=-0.48 p=0.002; six months: r=-0.48 p=0.02) and end-systolic volume (one week: r=-0.70 p<0.0001; six months: r=-0.64 p=0.001). The improvement of the noninfarcted area (from the first week to the sixth month) was only related to basal (one week) wall motion in this area (r=-0.58 p=0.003). We conclude that after an intermediate-large infarction, most patients exhibit a normal or hypokinetic noninfarcted area. Patients with a more depressed infarcted area show poorer contractility at the noninfarcted area. area exhibit greater progressive improvement.

Predictors of early and late ventricular remodeling after acute myocardial infarction.

BACKGROUND: The determinants of the early and late stages of the ventricular remodeling process after infarction are not well defined. HYPOTHESIS: The study was undertaken to evaluate the factors that condition the time course of left ventricular dilation during the first 6 months after infarction. METHODS: The study group consisted of 74 patients with a first intermediate-large (> or = 4 Q waves) acute myocardial infarction. Contrast left ventricular and coronary angiograms were performed at 7 +/- 1 and 175 +/- 25 days after infarction. Left ventricular volumes, regional function and infarction artery status were quantified. Percutaneous transluminal coronary angioplasty (PTCA) was performed in the early angiogram in 31 patients. RESULTS: In the early angiogram, 13 patients showed ventricular remodeling (end-diastolic volume > 90 ml/m2). A larger extent of dysfunction was the only predictor (p < 0.002) of early remodeling. At 6 months, a smaller, early end-diastolic volume (p < 0.0001) and a poorer regional function recovery (p < 0.05) were independently related to late diastolic enlargement, and a poorer regional function recovery (p < 0.0001) and a smaller, early end-systolic volume (p < 0.009) were independently related to late systolic enlargement. One patient with compared with 20 patients without early remodeling (p < 0.04) presented with late remodeling (increment of the end-diastolic volume > 20% at 6 months). In patients with early remodeling, the end-diastolic volume did not change significantly (101 +/- 13 vs. 94 +/- 22 ml/m2, NS) at 6 months; despite this, they maintained larger diastolic volumes than patients with late remodeling (81 +/- 12 ml/m2, p < 0.04) at 6 months. Infarction artery status did not influence the evolution of ventricular volumes and regional function. CONCLUSIONS: (1) A large infarct size is the main determinant of postinfarction remodeling. (2) Such infarct size-dependent ventricular dilation occurs early and does not tend to increase in late stage; in contrast, some cases of intermediate-large size infarcts without early remodeling exhibit late remodeling associated with a poor late recovery of regional function. (3) Recovery of regional function (indicating myocardial viability) rather than infarction artery status plays a role in the late ventricular remodeling process.

ST-segment elevation on Q leads at rest and during exercise: relation with myocardial viability and left ventricular remodeling within the first 6 months after infarction.

BACKGROUND: Resting ST-segment elevation on Q leads after an acute myocardial infarction has been related to a greater infarct size. Otherwise, the relation between exercise-induced ST-segment elevation and myocardial viability is controversial. We investigated the relation between ST-segment elevation on Q leads at rest and during exercise and regional dysfunction and its evolution, contractile reserve, left ventricular dilation, and coronary patency. METHODS AND RESULTS: Exercise testing and cardiac catheterization were performed at the first week after infarction in 51 patients. The study group was divided according to the existence (in 2 or more Q leads; n = 36) or not (n = 15) of resting ST-segment elevation and according to the existence (n = 28) or not (n = 23) of exercise-induced ST-segment elevation. Left ventricular end-diastolic and end-systolic volumes (mL/m2), regional wall motion (SD/chord), contractile reserve (wall motion percentage improvement with low-dose dobutamine), and coronary patency in the culprit artery were analyzed. Cardiac catheterization was repeated at the sixth month in 35 patients; systolic recovery (wall motion percentage improvement), left ventricular volumes, and coronary patency were again evaluated. Patients with resting ST-segment elevation showed poorer wall motion (2.1 +/- 0.8 SD/chord vs 1.2 +/- 1 SD/chord, P =.002), lesser contractile reserve (17% [0% to 39%] vs 41% [4% to 92%], P =.04), greater end-systolic volume (32 +/- 15 mL/m2 vs 23 +/- 11 mL/m2, P =.04), and higher percentage of occlusion (36% vs 7%, P =.04) than did patients without ST-segment elevation. Likewise, patients with exercise-induced ST-segment elevation showed lesser contractile reserve (8% [0% to 40%] vs 35% [12% to 86%], P =.03) than did patients without exercise-induced ST-segment elevation. The only independent predictors of contractile reserve were wall motion <2 SD/chord (odds ratio [OR] 7.1, confidence interval [CI] 6.3 to 7.9, P =.01) and the absence of exercise-induced ST-segment elevation (OR 5.7, CI 4.9 to 6.5, P =. 02). There were no significant differences between patients with and those without ST-segment elevation (at rest or during exercise) in systolic recovery or left ventricular volumes at the sixth month. CONCLUSIONS: ST-segment elevation on Q leads at rest is related to a poorer systolic function (more severe regional dysfunction, greater end-systolic volume, and less response to dobutamine). ST-segment elevation during exercise is independently related to a lesser contractile reserve. ST-segment elevation (at rest or during exercise) is not related to the evolution of volumes or regional dysfunction during the first 6 months after infarction.

Low-dose dobutamine testing using contrast left ventriculography in the same session as coronary angiography predicts the improvement of left ventricular function after coronary angioplasty in postinfarction patients.

The role of percutaneous transluminal coronary angioplasty (PTCA) in the subacute or chronic phases of myocardial infarction remains controversial. This study investigates the usefulness of dobutamine contrast left ventriculography in a single session with coronary angiography for predicting the improvement of ventricular function after PTCA. The study group consisted of 30 patients in whom a contrast left ventricular angiogram and PTCA were performed after a first myocardial infarction. The centerline method was used to calculate dysfunction extent at baseline and its variation during dobutamine infusion at 7.5 microg/kg/min; contractile reserve was defined as a significant (> or = 15%) reduction of dysfunction extent. A second ventricular angiogram was performed 6 months later in all patients. Abnormal wall motion extent decreased at 6 months after PTCA (84+/-21% vs 70+/-29%, p = 0.0001). Wall motion improvement after PTCA correlated with the response to dobutamine (r = 0.54, p = 0.002). Ten patients showed a significant reduction (> or = 15%) of dysfunction extent at 6 months; dobutamine testing had a 80% sensitivity, 84% specificity, 67% positive predictive value, and 89% negative predictive value in detecting regional function improvement. In the subgroup of 21 patients without restenosis, both the correlation between dysfunction improvement after PTCA and response to dobutamine (r = 0.72, p = 0.0001) and the accuracy of dobutamine testing (sensitivity 88%, specificity 92%, positive predictive value 88%, and negative predictive value 92%) increased. The ejection fraction significantly increased (>5%) after PTCA in 6 patients; dobutamine testing had a 67% sensitivity, 74% specificity, 44% positive predictive value, and 88% negative predictive value in predicting the increase in the ejection fraction. In the subgroup without restenosis the improvement of the ejection fraction correlated with the response to dobutamine (r = 0.63, p = 0.007), and the sensitivity of dobutamine testing was 80%, specificity 83%, positive predictive value 67%, and negative predictive value 91%. In conclusion, dobutamine contrast left ventriculography testing in the same session as coronary angiography predicts regional function and ejection fraction improvement after PTCA in postinfarction patients, particularly when restenosis does not develop.

[Wiktor coronary stent for elective placement with an antiaggregation regimen. WINE study. WINE Group Study]. / Stent coronario Wiktor por indicación electiva con régimen de antiagregación. Estudio WINE. Grupo de Estudio WINE.

INTRODUCTION AND OBJECTIVES: The main problems associated with coronary stent implantation are subacute thrombosis and vascular and hemorrhagic complications due to the intensive anticoagulant regime. We studied the complications and the six-month restenosis rate after the elective implantation of a Wiktor stent in patients treated only with antiplatelet drugs. PATIENTS AND METHODS: The WINE study is an open, observational, multicenter study that included 368 patients (380 lesions) from 11 Spanish hospitals. All patients were treated with aspirin (125-325 mg/day) and ticlopidine (250 mg/12 h for 4 weeks). After hospitalization, a clinical control and clinical and angiographic controls were performed at one and six months respectively. RESULTS: 27 patients were excluded after the procedure because of failed delivery of the stent (5 cases), suboptimal angiographic result (15 cases) or lack of adherence to the antithrombotic regime (7 cases). Among the 341 patients with an adequate result most lesions (76.2%) were type B, including 39.1% type B2 and 8.5% type C. Subacute stent occlusion occurred in two patients (0.6%). Seven patients (2.1%) had vascular complications related to the arterial puncture. No major hemorrhagic complications needing transfusion were found. At six months 64 patients (19.8%) showed angiographic restenosis. CONCLUSIONS: When the angiographic result after Wiktor stent placement is adequate, the therapy with aspirin and ticlopidine is associated with a very low stent thrombosis rate as well as with a low rate of vascular complications and 6 month angiographic restenosis.

Role of infarction artery status in left ventricular remodeling after acute myocardial infarction.

The aim of this study was to evaluate the relation between the infarction artery status and left ventricular volumes, independently of regional ventricular dysfunction, at 4-6 weeks after a first myocardial infarction. The study group consisted of 100 patients, of whom 80 received thrombolytic treatment. Coronary and contrast left ventricular angiograms were performed at 36+/-5 days postinfarction. Left ventricular end-diastolic and end-systolic volumes were measured. The centerline chord motion method was used to calculate the extent of wall motion abnormality (percentage of chords with hypokinetic motion) and its severity (maximum units of S.D. below the normal wall motion reference). Minimum lumen diameter, patency and collateral flow in the infarction artery were also analyzed. Eight patients (group I) showed occlusion with poor collateral flow in the infarction artery, 22 patients (group II) occlusion with good collateral flow, 38 patients (group III) severe residual stenosis (minimum lumen diameter < or = 1 mm), and 32 patients (group IV) non-severe residual stenosis (minimum lumen diameter > 1 mm). Patients from group I presented greater wall motion abnormality in terms of both extent (P=0.005) and severity (P=0.007), and greater end-diastolic (P=0.07) and end-systolic (P=0.0008) volumes; there were no differences among groups II, III and IV. By stepwise multivariate regression analysis, the extent of wall motion abnormality was the main determinant of end-diastolic (P=0.0001) and end-systolic (P=0.0001) volumes; occlusion with poor collateral flow was also a significant independent factor for end-systolic volume (P=0.03). Total occlusion (including both with and without collaterals) and the minimum lumen diameter did not correlate with end-diastolic and end-systolic volumes. We concluded that (A) the extent of regional dysfunction is the primary determinant of left ventricular volumes at 4-6 weeks postinfarction. (B) The status of the infarction artery is a weak predictor of end-diastolic volume, which is the best descriptor of ventricular remodeling, although occlusion with poor collateral flow is associated to larger end-systolic volume.

[Persistence of the left superior vena cava associated with aortic insufficiency: diagnostic and therapeutic considerations]. / Persistencia de la vena cava superior izquierda asociada a insuficiencia aórtica: consideraciones diagnósticas y terapéuticas.

In the course of the routine evaluation of a 26-years-old male for acquired aortic valve disease the persistence of a left superior vena cava draining into the coronary sinus was detected. This is a frequent congenital malformation of the systemic venous system that has no hemodynamic consequences in itself, though it may be associated to other congenital or acquired cardiac malformations that may require surgery. The preoperatory detection of the anomaly prevents unexpected problems when connecting the cardiopulmonary bypass. We emphasize the importance of procedures that suggest the diagnosis and characterize the anatomo-functional nature of the condition--including transthoracic and transesophageal echocardiography using echocardiographic contrast, and cardiac catheterization with cardiac and vascular angiography.

Stunned myocardium after thrombolytic treatment. Identification by dobutamine echocardiography and role of the residual stenosis in the infarction artery.

UNLABELLED: The aim of this study was to identify post-thrombolysis stunned myocardium using low dose (10 micrograms/kg/min) dobutamine echocardiography, and to elucidate the role of the residual stenosis in the infarction artery in wall motion recovery. Forty-seven consecutive patients treated with thrombolytic agents for a first non-complicated myocardial infarction were included. An early dobutamine echocardiogram was performed 7 +/- 2 days after thrombolysis to calculate a wall motion score index at baseline and with dobutamine. A late resting echocardiogram 36 +/- 7 days and a coronariography 41 +/- 8 days after thrombolysis were also performed. In 12 patients no baseline regional dysfunction was observed in the early echocardiogram (Group I), whereas 35 patients (Group II) presented regional dysfunction which improved with dobutamine in 11 cases (Group IIA), but not in 24 (Group IIB). Maximum creatine kinase peak was smaller in Group I (458 +/- 162, P < or = 0.01) and in Group IIA (931 +/- 593, P < or = 0.05) than in Group IIB (1547 +/- 886). Late resting echocardiogram was performed in 44 patients: all 12 from Group I, 10 from Group IIA and 22 from Group IIB; all patients from Group I persisted with normal wall motion, while the baseline score index improved in seven patients (70%) from Group IIA vs. three patients (14%) from Group IIB (P < or = 0.01). Quantitative angiographic parameters in the infarction artery failed to differentiate the subgroup of patients in whom wall motion improved in the late echocardiogram. By simple regression, smaller creatine kinase peak (P < or = 0.05) and a positive response to dobutamine in the early echocardiogram (P < or = 0.001) correlated with wall motion recovery, but the minimum lumen diameter in the infarction artery did not correlate; by multiple logistic regression, only a positive response to dobutamine in the early echocardiogram independently predicted late wall motion improvement (P < or = 0.001). CONCLUSIONS: (1) Low dose dobutamine echocardiography early after thrombolytic treatment identifies dysfunctional myocardium with potential late spontaneous improvement (stunned myocardium). (2) Myocardial stunning tends to occur in small infarctions. (3) Late wall motion improvement can occur despite severe residual stenosis in the infarction artery.

[Apical hypertrophic myocardiopathy and multiple fistulae between the coronary vessels and the left ventricle]. / Miocardiopatía hipertrófica apical y múltiples fístulas entre coronarias y ventrículo izquierdo.

A male patient presented with symptoms of angor under effort. Echocardiography and angiocardiography revealed apical hypertrophic myocardiopathy, associated with multiple fistulas connecting the anterior descending coronary artery and right coronary artery with the cavity of the left ventricle, as demonstrated by coronariography. We comment on the hypothesis that support a causal relationship between the two anomalies, microfistulas being the possible cause of the reactive hypertrophy through the induction of a coronary steal phenomenon with local ischemia; alternatively, the myocardiopathy itself might be the cause of microfistulas formation by inducing an anomaly in the Thebesius venous system. A pathogenic relationship is suggested between the syndrome of angor and these two rare pathological entities.

Function of atrioventricular node conduction: hyperbolic model.

Twenty four patients were subjected to an electrophysiologic clinical procedure. The conventional extrastimulus test was applied to verify the relation between conduction time increase through the atrioventricular node of the extrastimulus beat (delta AH), and its preceding interval (A1A2). Following the least square root method the parameters of the hyperbolic model delta AH.A1A2 = m . delta AH + n were adjusted. The correlation coefficients obtained and tested in all cases were very high and significant. From this hyperbolic equation it was possible to determine the equations for the effective refractory period (ERPe = m) and functional refractory period (FRPe = ERPe + n). The theoretical values for refractoriness approached very closely those of the actually measured ERP and FRP, in all cases. This model proved to be, in respect to adjustments and especially in calculating refractory periods, at least as good as the exponential model proposed previously by other authors.