[Reliability of digital coronary quantification in a hemodynamic laboratory. Comparison with a film-based system]. / Fiabilidad de la cuantificación coronaria digital realizada en el laboratorio de hemodinámica. Comparación con un sistema basado en película.

BACKGROUND AND OBJECTIVES: Quantitative coronary angiography can be performed in two ways: on-line during catheterism, and off-line once the procedure is finished. Consequently, several studies have been published comparing both systems. Nevertheless, none of them has compared the measurements made off-line with those acquired on-line by the hemodynamist in charge of procedure. The objective of this study was to compare the measurements made on-line by the hemodynamist involved in the procedure with a digital system (DCI) with those obtained off-line by an independent and alien observer to the procedure by using film-based system (CMS). MATERIAL AND METHODS: Forty coronary lesions suitable for quantification were measured in a prospective fashion. They came from follow-up angiograms. Either balloon or stent were used in the previous angioplasty. Stenoses were assessed on-line and off-line by using the most severe view as judged by the hemodynamist. RESULTS: No significant differences were found for obstruction diameter, reference diameter nor percent diameter stenosis. Pearson's correlation coefficient values (r), intraclass correlation coefficient (ri), regression line equation and mean of signed differences with their standard deviations are showed: a) obstruction diameter: r = 0.83, ri = 0.83, DCI = 0.42 + 0.76 x CMS, -0.01 +/- 0.42 mm; b) reference diameter: r = 0.72, ri = 0.69, DCI = 1.29 + 0.61 x CMS, 0.003 +/- 0.38 mm, y c) percent diameter stenosis: r = 0.86, ri = 0.86, DCI = 10.05 + 0.77 x CMS, 1.19 +/- 10.75%. CONCLUSIONS: We attained good concordance between both quantification systems under clinical conditions. In our opinion these results support the use of on-line quantification as a reliable tool for clinical decision making in the catheterization laboratory.

Mechanism and location of atrial flutter in transplanted hearts: observations during transient entrainment from distant sites.

OBJECTIVES: This study was designed to elucidate the location and mechanism of typical atrial flutter in the transplanted heart. BACKGROUND: Although the F wave morphology in atrial flutter is similar in nontransplanted and transplanted hearts, the surgical incision needed for the atrial anastomosis may create a distinct electrophysiologic substrate of atrial flutter. METHODS: Entrainment from the lateral wall of the right atrium and interatrial septum was used to determine the location of atrial flutter in five patients with a transplanted heart and six patients with a nontransplanted heart. The difference between the first postpacing interval (FPPI) and the flutter cycle length (FCL) was used as an index of proximity to the circuit. RESULTS: In the transplant group, the FPPI was equal to the FCL at sites located close to the tricuspid annulus (TA); the mean differences (+/-SD) were 1 +/- 5 and -1 +/- 2 ms at the lateral wall and interatrial septum, respectively. However, from sites close to the surgical incision at the lateral wall and at the interatrial septum, these differences were significantly longer (29 +/- 12 and 27 +/- 9 ms, respectively, p < 0.05). In the nontransplant group, the FPPI was similar to the FCL at points in the lateral wall and interatrial septum close to the TA (mean difference 7 +/- 6 and 6 +/- 11 ms, respectively) and at sites close to the crista terminalis (CT) in the lateral wall (mean difference 4 +/- 4 ms). However, in sites separated from the TA at the interatrial septum the difference was markedly longer (35 +/- 11 ms, p < 0.05). CONCLUSIONS: Atrial flutter in transplanted hearts may best be explained by macroreentry around the tricuspid ring. In non-transplanted hearts a different structure (perhaps the CT?) may be the basis for atrial flutter at the lateral wall.

[Etiopathogenesis and classification of dilated cardiomyopathy]. / Etiopatogenia y clasificatión de la miocardiopatía dilatada.

Dilated cardiomyopathy is a diffuse disease of the myocardium, with systolic dysfunction and ventricular enlargement which is clinically expressed as heart failure and sudden death. A variety of etiologies, including myocardial diseases produced by specific local or systemic disorders can cause this syndrome. The etiological diagnosis is very difficult in the clinical setting. Because the progression of the disease is potentially reversible, discovering the cause, if possible, seems very interesting. The basic pathogenic mechanisms are not well known. The different etiopathogenic hypotheses, viral, immunological, genetic, and toxic are not incompatible and may even be complementary. Research through immunogenetical and molecular biology techniques is the key to understanding the basic mechanisms. The usefulness of genetic therapy is under investigation.

[Graft vascular disease. Its pathogenesis and diagnosis]. / Enfermedad vascular del injerto. Patogenia y diagnóstico.

Transplant coronary artery disease (EVI) is still the leading cause of late mortality in cardiac transplant patients. The pathogenesis is not determined yet. Probably the basic mechanism is immunological but the subsequent development and progression of the disease depend on the interaction of immunological and nonimmunological factors. Its typical diffuse morphology and its behavior make difficult the diagnosis with non invasive methods. Coronary angiography is not sensitive for an early diagnosis of EVI but its detection has prognostic value. Intracoronary ultrasound (IVUS) is very sensitive to detect angiographically silent lesions, and has correlated well with histological findings. Its prognostic value is still being evaluated. More studies are needed to establish the usefulness of endothelial dysfunction and coronary flow reserve tests in the evaluation of EVI.

[Primary coronary angioplasty in acute anterior myocardial infarction: immediate results]. / Angioplastia primaria en el infarto agudo de miocardio de localización anterior: resultados inmediatos.

BACKGROUND: Some reports have indicated that primary angioplasty not contaminated by previous intravenous infusion of thrombolytic agents represents an efficient approach to the treatment of acute myocardial infarction. PATIENTS AND METHODS: As a part of a more ambitious protocol aiming to compare primary angioplasty and intravenous recombinant tissue plasminogen activator, we performed direct coronary angioplasty in 33 patients (18 randomized to angioplasty and 15 because of contraindication to thrombolysis) that were admitted to our hospital with acute myocardial infarction with less than 5 hours elapsed from the onset of pain and with clear electrocardiographic criteria of anterior infarction. RESULTS: In 30 of the 33 patients (90.9%) the left anterior descending artery was recanalized and TIMI 2 flow in 17 and 3 in 13 was obtained. The average time elapsed from the onset of pain to the opening of the artery was 228 +/- 70 (120-390) minutes and from the time of admission to the coronary care unit to complete reperfusion 91 +/- 43 minutes (33-120). Thirty one patients (93.9%) were discharged from the hospital and two (6.1%) died. There was only one hemorrhagic complication without sequelae. CONCLUSIONS: Primary coronary angioplasty in acute anterior myocardial infarction is an efficient, safe and not so difficult therapeutic strategy. Even though it requires a complex around the clock on call set up it is specially useful in specific subsets of patients.

Emergency coronary stenting for acute occlusive dissection of the left main coronary artery.

Catheter-induced left main coronary artery dissection is a rare but serious complication of diagnostic cardiac angiography. We report the case of a patient with mitral regurgitation and accidental dissection of the left main coronary artery successfully managed with intracoronary stent that allowed emergent surgical revascularization and mitral replacement.

[Experience with the Palmaz-Schatz stent in the treatment of postangioplasty coronary dissection]. / Experiencia con el stent de Palmaz-Schatz en el tratamiento de la disección coronaria postangioplastia. Resultados a corto y medio plazo.

Some authors have proposed the use of coronary stenting as a good therapeutic strategy for post angioplasty acute coronary dissection. We present our experience with the Palmaz-Schatz stent for the treatment of acute coronary dissection after percutaneous coronary angioplasty. Twenty five stents were deployed in nineteen patients with occlusion (7) or threatened occlusion (12). Eleven patients (58%) had multivessel disease, seven (37%) unestable angina and six (32%) previous myocardial infarction. The attempted lesion was type A in four patients (21%), type B in thirteen (68%) and type C in two (11%) according to the American College of Cardiology/American Heart Association classification. To cover the dissection was necessary to deploy three stents in two patients, and two stents in two more. The other fifteen patients received one stent each. In eighteen patients (95%) the stent deployment was accomplished with immediate angiographic success. Twelve stents were deployed in the right coronary artery, eight in the left anterior descending and five in the circumflex. In sixteen patients (84%) the stent successfully solved the occlusion or threatened occlusion reassuming a normal coronary flow. There were 10 complications in six patients: one death (5%), 3 cases of emergency coronary artery bypass graft (16%), 2 acute myocardial infarction (11%), 2 hemorrhagic complications (11%) and 2 cases of subacute thrombosis of the stent (11%). The Palmaz-Schatz stent seems to be a useful tool for the management of acute coronary dissection with a fair number of complications. The results obtained during hospitalization are maintained with a more than acceptable restenosis rate.

[Problems in the interpretation of changes in the ST segment after emergency cardioversion]. / Problemas en la interpretación de las alteraciones del segmento ST tras la cardioversión de urgencia.

After cardioversion with continuous current (CV) we can find alterations in the ST segment and T wave, frequently associated with an increase in CPK total and CPKmB, which can lead us to the wrong diagnosis of acute myocardial infarction (AMI). We describe five cases of transitory alterations in ST after CV: four regular tachycardias with wide QRS and an atrial fibrillation with fast ventricular response. CPK, CPKmB and ECG were monitored being the CPK abnormal in all cases. AMI was discarded in all cases. When changes in ST following CV are observed, we believe that AMI should be discarded by ECG and enzymatic monitorization. If doubts persist technetium-99mm pyrophosphate must be used.

[Experience with a protocol of systematic postfibrinolysis angioplasty in acute myocardial infarct]. / Experiencia con un protocolo de angioplastia sistemática posfibrinólisis en el infarto agudo de miocardio.

Two hundred twenty one patients admitted for AMI in the CCU, and treated with systemic thrombolysis with streptokinase have been retrospectively analysed and divided in two groups: the first 98 patients (group A) were included in a research protocol: The following 123 patients (group B) represent the clinical application of thrombolytic therapy in our unit. In group A coronary arteriography in the first 48 hours (84 patients), and PTCA to the infarct related artery with significant stenosis (39 patients) were performed systematically. In group B, 54 patients had coronary arteriography PTCA was restricted to 12 patients with symptomatic ischemia. No significant differences in base line clinical parameters were detected between groups A and B. Total hospital mortality was 5% and similar in both groups. Reinfarction rate was greater in group A, 13% than in group B, 5%, but not significantly different. Reinfarction was related to PTCA (chi 2 test p less than 0.05). The incidence of post infarction angina was related to the existence of more than one diseased vessel. These data suggest that protocol PTCA post thrombolysis is not effective in reducing post infarction ischemia or mortality.