Luis Insa

Pronóstico a corto plazo de los pacientes ingresados por probable síndrome coronario agudo sin elevación del segmento ST. Papel de los nuevos marcadores de daño miocárdico y de los reactantes de fase aguda

Objectives. The relative value of classic markers, myocardial damage variables, and levels of acute-phase reactants in establishing the pre-discharge prognosis of acute coronary syndrome without ST-segment elevation was analyzed. Method. We prospectively studied 385 consecutive patients admitted from our chest pain unit with a highprobability diagnosis of acute coronary syndrome without ST-segment elevation. The clinical and electrocardiographic data, myocardial damage markers (troponin I, CK-Mb mass, myoglobin), and acute-phase reactants (high-sensitivity C-reactive protein, fibrinogen) were recorded. Results. During admission, 15 deaths (3.9%) and 16 complicative infarctions (4.2%) occurred, for a total of 31 major events (death and/or infarction: 8.1%). Age (p = 0.03), insulin-dependent diabetes (p = 0.009), and C-reactive protein (p = 0.05) were independently related to death. Fibrinogen was related to infarction (p = 0.01); by fibrinogen quartiles: 1.4%; 1.4%; 2.9%, and 11.7% (p = 0.02). Age (p = 0.01), insulin-dependent diabetes (p = 0.02), and C-reactive protein (p = 0.04) were independent predictors of major events; by C-reactive protein quartiles: 1.4%; 5.5%; 5.4%, and 16.7% (p = 0.004). Troponin I was related to major events (p = 0.03), but it was not an independent predictor. Conclusions. Acute-phase reactants add independent information to clinical variables in the short-term risk stratification of patients with an acute coronary syndrome. The predictive power of troponins is lower than that of

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.

Resultados iniciales y seguimiento clínico a 6 meses tras el implante de un stent coronario recubierto de carburo de silicio

Introduccion y objetivos Presentar la experiencia inicial en Espana con el stent coronario Tenax, de acero inoxidable 316L recubierto de una capa de carbono de silicio amorfo rico en hidrogeno. Pacientes y metodos Desde julio de 1998 a julio de 1999 se implantaron 231 stents Tenax® en 206 pacientes de 9 centros (62 ± 5 anos) como unico procedimiento revascularizador. La indicacion clinica mas frecuente fue la angina inestable (66%), siendo la mayoria de las lesiones complejas (clases B2 y C). La arteria mas revascularizada fue la descendente anterior (51%). La fraccion de eyeccion fue inferior a 0,5 en 19% de casos. El resultado inmediato se valoro con angiografia cuantitativa y el seguimiento a 6 meses fue clinico. Resultados La revascularizacion fue completa en el 70%, electiva en el 80% y con implante directo en el 25% de los casos. El stent se desplego con exito en todos los pacientes. La estenosis disminuyo del 62 ± 16 al 16 ± 10% y el diametro luminal minimo aumento de 0,81 ± 0,40 a 2,61 ± 0,59. El flujo TIMI, comprometido en un 30% de casos, se normalizo en todos menos un caso. La incidencia de acontecimientos cardiacos fue minima: una trombosis aguda (0,5%) resuelta con nueva angioplastia y un infarto agudo de miocardio sin onda Q (0,5%). A los 6 meses reaparecio angina mayor de clase II en el 10% de los pacientes y se realizo una nueva angioplastia en el 1,9% de los casos. Conclusiones Los datos clinicos y angiograficos sugieren que el recubrimiento del stent coronario Tenax con carburo de silicio hidrogenado posiblemente desempena un papel beneficioso en el porvenir de los pacientes, aunque requiere una evaluacion en estudios clinicos prospectivos.

Implications of the ''Watermelon Seeding'' Phenomenon During Coronary Interventions for In-Stent Restenosis

The occurrence of balloon slippage (“watermelon seeding”; WMS) during treatment of patients with in‐stent restenosis (ISR) has been described, but predisposing factors and the potential implications of this phenomenon remain unknown. In the Restenosis Intrastent: Balloon Angioplasty vs. Elective Stenting (RIBS) randomized study, 450 patients with ISR were included. Of these, 42 patients (9%) presented WMS during the procedure. WMS was detected in 26 patients (12%) in the balloon arm and 16 (7%) in the stent arm (P = 0.11). In the stent arm, WMS was only noticed during balloon predilation, never during stent implantation. As compared with 408 patients without WMS, patients with WMS had more severe (TIMI flow 1; 21% vs. 8%; P = 0.01) and diffuse (length > 15 mm: 45% vs. 28%; P = 0.02) ISR lesions. Patients with WMS required more balloon inflations, longer total inflation time, had more frequent crossover to stenting or ended the procedure with residual dissections, and eventually obtained poorer acute results (minimal lumen diameter, 2.35 ± 0.5 vs. 2.53 ± 0.5 mm; P = 0.03). In addition, at 6‐month follow‐up, patients with WMS had a smaller minimal lumen diameter (1.26 ± 0.7 vs. 1.61 ± 0.7 mm; P = 0.007) and a higher restenosis rate (56% vs. 37%; P = 0.017). On logistic regression analysis, the WMS phenomenon emerged as an independent predictor of recurrent restenosis (adjusted RR = 2.1; 95% CI = 1.1–4.1; P = 0.04). The WMS phenomenon may complicate treatment of patients with ISR. Long and severe lesions appear to predispose to this technical problem that never occurs during stent deployment. In patients with ISR, WMS is associated with cumbersome procedures and poorer acute and long‐term angiographic results.

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.

Factores pronósticos en la angina inestable con cambios dinámicos del electrocardiograma. Valor del fibrinógeno

Introduction and objectives. The prognosis of unstable angina varies between series depending on the inclusion criteria and management protocol used. The aim of this study was to analyze in-hospital events and their predictors in a homogeneous single-center series of patients with unstable angina. Material and methods. A total of 246 patients with the following inclusion criteria were studied: 1) resting anginal pain, 2) transient electrocardiographic changes during anginal pain, 3) normal CK-MB levels and 4) exclusion of postinfarction angina. All patients were treated with aspirin and enoxaparin (1 mg/kg/12 h). Coronary angiography was performed in the case of recurrent angina or ischemia in Bruce I-II stage during the predischarge effort stress test. The variables recorded were risk factors, history of ischemic heart disease, history of coronary surgery, ECG upon admission, and fibrinogen. Results. During the hospital stay the following events were recorded: 36% recurrent angina, 58% cardiac catheterization, and 5,7% major events (infarction or death). Multivariate analysis found recurrent angina to be more frequent in patients with a history of coronary bypass surgery (p = 0.004. OR = 22; CI 95%, 3-182), ST-segment changes (p = 0.01. OR = 4.7, CI 95%; 1.4-15.9) and higher fibrinogen (p = 0.002. OR = 1,4, CI 95%; 1.1-1.7). Fibrinogen was the only variable related to cardiac catheterization (p = 0,009. OR = 1.3. CI 95%, 1.1-1.6) and major events (p = 0.001. OR = 2.0. CI 95%, 1.4-3.1). Conclusions. 1) Unstable angina with electrocardiographic changes was associated to a high rate of in-hospital events. 2) Fibrinogen was related to any event, and previous by-pass surgery and ST changes were related to recurrent angina.

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.

The EXTREME registry: Titanium-nitride-oxide coated stents in small coronary arteries†

Objectives: We sought to explore the immediate results of Titan2® stent implantation in small coronary arteries, as well as the incidence of major adverse cardiac events (MACE) at six months follow‐up. Background: The safety of Titan2® stent has been confirmed in several studies in real‐life unselected populations. Methods: We enrolled 311 consecutive patients admitted for percutaneous intervention for at least one significant (50%) de novo lesion in a native small coronary artery (2.0–2.75 mm). All lesions were treated with Titan2® stent implantation. Patients were prospectively followed up for at least six months. The primary endpoint was MACE at six months follow‐up [death, myocardial infarction (MI), or target vessel revascularization (TVR)]. Secondary endpoints included angiographic and clinical procedural success, in‐hospital MACE, target lesion revascularization (TLR) during follow‐up, and stent thrombosis. Results: The mean age was 67.3 ± 10.9 years (65.9% males). A total of 356 Titan2® stents were implanted in 353 lesions. Angiographic and clinical procedural success was achieved in 344 (97.5%) patients. No case of in‐hospital MACE or acute stent thrombosis was reported. Clinical follow‐up was completed for an average of 8 ± 2 months. Two patients (0.7%) died, and 6 (2.1%) developed MI. TLR was performed in 12 (4.2%) and TVR in 16 (5.5%) patients, all were clinically driven. Cumulative MACE occurred in 20 (6.9%) patients. One patient suffered subacute stent thrombosis, but no late stent thrombosis. Conclusions: Titan2® stent implantation in small coronary arteries achieves excellent immediate outcome, with a low incidence of MACE at mid‐term follow‐up.

Persistent truncus arteriosus type 4 with survival to the age of 54 years

We describe a case of persistent truncus arteriosus type 4 in an unrepaired 54-year-old woman with the peculiarities of long survival, absence of pulmonary arteries and good clinical status.

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.