Third-degree inter-atrial block and supraventricular tachyarrhythmias.
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Atrial Function, Left↗
Biomedical subjects
A Bayés-Genís
Publications and source records attributed to A Bayés-Genís.
Elevated levels of plasmin-alpha2 antiplasmin complexes in unstable angina.
The evidence of elevated levels of several biochemical markers of prothrombotic state in patients with unstable angina suggests that thrombus formation and lysis play a pivotal role in acute coronary syndromes. The clinical syndrome of unstable angina encompasses a variety of clinical presentations of transient episodes of myocardial ischemia. This study was designed to assess plasmin generation in different settings of unstable angina. Evidence of plasmin generation in patients with unstable angina was measured by circulating plasmin-alpha2 antiplasmin complexes (PAP). A second objective was to identify whether PAP levels had a prognostic value to predict outcome. Eighty-five patients admitted to the coronary care unit for unstable angina were classified into three groups. Group A included 26 patients with postinfarction angina; group B comprised 26 patients with new onset angina; and group C included 33 patients with crescendo angina. Mean PAP levels were higher in the three groups compared to healthy controls. A significant correlation was found between levels of PAP and D-dimer, particularly in postinfarction angina (r = 0.6; p <0.0005). This trial adds new insights into the pathophysiology of unstable angina. It demonstrates that plasmin is generated in the different settings of unstable angina but particularly in postinfarction angina patients where a fibrin-rich thrombus is responsible of the symptoms. However, in this series PAP levels do not predict an uneventful outcome neither in the acute phase nor at long term (6 months).
Aged↗
[Initial results with the Multi-Link coronary stent].
INTRODUCTION AND OBJECTIVES: The Multi-Link intracoronary stent is a balloon-expandable stainless steel stent with an interconnected ring structure designed to provide a high degree of compressive resistance while preserving longitudinal flexibility. We present the results of our initial experience with the implantation of this stent. PATIENTS AND METHODS: From May 1996 to April 1997, 124 Multi-link stents were implanted in 97 patients. Mean age 62.2 +/- 11 years. All patients included had a coronary artery diameter > 2.7 mm. Clinical presentation includes stable angina in 20, unstable angina in 72, and myocardial infarction in 5 patients. According to the ACC/AHA classification 6 lesions were type A, 72 type B and 19 type C. The implantation of the stent was for "de novo" lesions in 85 patients and for restenosis in 12. Patients were treated after the procedure with a combination of aspirin and ticlopidine, except six of them who received aspirin and acenocumarol. 16 patients were treated additionally with Abciximab. The degree of stenosis was determined by quantitative angiography. RESULTS: The delivery of the stent was successful in all patients. The degree of stenosis before the procedure was 79.6 +/- 13.1%, and after the stent deployment was 17.7 +/- 11.4%. Three patients presented a non-Q-wave myocardial infarction, two patients had a subacute stent thrombosis, one of them died due to heart failure. During a follow-up of 4.7 +/- 2.6 months five patients were readmitted with recurrent angina (4 due to restenosis and one for vessel occlusion) and one patient with heart failure after myocardial infarction died suddenly three weeks after the dilatation. CONCLUSIONS: The Multi-Link stent was implanted successfully in all patients with a low incidence of complications, showing at the follow-up a reduced rate of clinical restenosis.
Coronary Disease↗
[Tricuspid and pulmonary valve in a case of carcinoid syndrome].
The presence of liver methastasis and serotonin in plasma in the carcinoid tumor are responsible for the carcinoid syndrome. We present a case of tricuspid and pulmonary valvular disease secondary to this syndrome. The finding of liver hyperechogenic nodules added to the described valvular disease by subcostal echocardiogram oriented the diagnosis.
Female↗
Cardiac arrhythmias and left ventricular hypertrophy in systemic hypertension and their influences on prognosis.
Left ventricular hypertrophy (LVH) is the adaptative mechanism of the heart to systolic overload of the left ventricle. Nevertheless, LVH plays a role in some complications, such as cardiac arrhythmias. Patients with LVH are more likely to develop ventricular arrhythmias than the hypertensive population without LVH. Further, the relation between left ventricular mass and ventricular arrhythmias is graded and continuous. The arrhythmias described in hypertensive patients with LVH are usually isolated premature ventricular contractions. The presence of electrocardiographic criteria of LVH represents a risk of higher incidence of sudden death, especially in men. The risk is even greater in the presence of ventricular arrhythmias. The presence of late potentials has been recently characterized as more related to ventricular arrhythmias than LVH. Antihypertensive drugs that can reduce LVH also have a beneficial effect on cardiovascular morbility and mortality.
Antihypertensive Agents↗
Electrocardiographic and clinical precursors of ventricular fibrillation: chain of events.
Ventricular fibrillation is the final event in the majority of cases of sudden death. The ECG and clinical precursors of ventricular fibrillation are discussed in this article. Ventricular fibrillation usually appears as a consequence of a chain of events that leads to the appearance of this lethal arrhythmia. We review the markers of the vulnerable myocardium prone to ventricular fibrillation, the triggers and modulators that act on this vulnerable myocardium, and the event(s) that constitute the final step preceding this arrhythmia. The final step may be as unique as a sudden waterfall or present as a cascade of successive phenomena.
Electrocardiography↗
Effects of progestogens on thrombosis and atherosclerosis.
In contrast with past practice, current hormone replacement usually includes a combination of oestrogens and progestogens. In this article, we review the effect of progestins on haemostasis and in the development of atherosclerosis. Second-generation progestogens produce minor haemostatic changes, and in lipid metabolism they decrease the synthesis of triglycerides and very low density lipoproteins (VLDL) and stimulate hepatic lipoprotein lipase. In combination, progestogens modify the effect of oestrogens on hepatic metabolism, endothelium and platelets. Several new progestins (known as third-generation) have less effect on lipid profiles. In vessel walls, animal studies have shown that progestogens are able dose-dependently to inhibit the beneficial effect of oestrogen without significant changes in lipid concentrations. The endothelium-dependent vasoconstrictor effect of progestogens on the arterial wall has been also evaluated. Large epidemiological studies show a two-fold increase in risk of venous thromboembolism with the use of third-generation progestins. Regarding the risk of myocardial infarction, no definite evidence is yet available with the use of third-generation progestins. The clinical consequence is therefore that second-generation progestins are the first choice in prescription for first-time users.
Animals↗