[C-reactive protein as a coronary risk factor].
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Biomedical subjects
Publications and source records attributed to J Guindo.
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INTRODUCTION: There is scant information about the effects of thrombolysis in the evolution of right bundle-branch block (RBBB) in the setting of acute anterior myocardial infarction. The aim of this study has been to analyse these effects and its impact on prognosis. METHODS: We studied 54 patients who presented a RBBB related to an acute anterior myocardial infarction. We defined two groups: those who received thrombolytic treatment and those who did not. We analysed the evolution of RBBB (transience, moment of onset, moment of disappearance) and its relationship with in-hospital mortality.Twenty-one patients (39%) received thrombolytic treatment (groupT) and 33 patients (61%) (group NT) did not. RESULTS: The incidence of late appearance (> 6 h) of RBBB was less frequent in group T compared with group NT (10% vs. 33%, p = 0.04). The incidence of transient block was similar in the two groups (57% vs. 45%, p ns). However, early disappearance of RBBB (in < 6 hours) was more common in group T than in group NT (33% vs. 9%, p = 0.04). Mortality was higher in patients with RBBB present at 24 h after admission) than in those with RBBB resolved in less than 24 hours (in group NT, 55% vs. 8%, p = 0.02 and in group T 50% vs. 0%, p = 0.02, respectively). CONCLUSIONS: Thrombolysis seems to influence the moment of onset and disappearance of RBBB by promoting its early disappearance and avoiding its late appearance. Disappearance of RBBB is associated with a better prognosis.
BACKGROUND: Chest pain is a frequent symptom in the emergency department and often presents a diagnostic challenge. Because coronary thrombosis is a hallmark of acute ischemic syndromes, the substrates of the coagulation and fibrinolysis cascades may be markers of coronary ischemia. The objective of this study was to determine the diagnostic value of several hemostatic markers in patients presenting to the emergency department (ED) with chest pain syndromes. METHODS: Two hundred fifty-seven consecutive patients with acute chest pain were studied in this prospective study conducted in an urban ED. D-Dimer levels were measured at admission to the ED in all patients. We also measured thrombin-antithrombin complexes, prothrombin fragment 1+2, activated factor VII, and fibrinogen. We used regression analysis to estimate the likelihood of myocardial infarction and the diagnostic value of D-dimer. RESULTS: D-Dimer and fibrinogen levels were significantly higher in patients with acute ischemic events (myocardial infarction and unstable angina) than in nonischemic patients (P <.01 and P =.02, respectively). The other hemostatic markers were not significantly elevated in patients with ischemic events. D-Dimer level >500 microg/L had an independent diagnostic value for myocardial infarction and increased the diagnostic sensitivity of the electrocardiogram and history from 73% to 92%. CONCLUSION: D-Dimer, an expression of ongoing thrombus formation and lysis, is a marker of substantial incremental value for the early diagnosis of acute coronary syndromes presenting with chest pain. It adds independent information to the traditional assessment for myocardial infarction. D-Dimer can be incorporated into clinical decision models in the ED.
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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).
BACKGROUND: The most troublesome complication of acute pericarditis is recurrent episodes of pericardial inflammation, occurring in 15% to 32% of cases. The cause of the recurrence is usually unknown, although in some cases it may be traced to viral infection or may be a consequence of coronary artery bypass grafting. The optimal method for prevention has not been fully established; accepted modalities include nonsteroidal anti-inflammatory drugs, corticosteroids, immunosuppressive agents, and pericardiectomy. METHODS AND RESULTS: Based on the proven efficacy of colchicine therapy for familial Mediterranean fever (recurrent polyserositis), several small studies have used colchicine successfully to prevent recurrence of acute pericarditis after failure of conventional treatment. Recently, we reported the results from the largest multicenter international study on 51 patients who were treated with colchicine to prevent further relapses and who were followed up for < or = 10 years. CONCLUSIONS: In light of new trial data that have accumulated in the past decade, we review the evidence for the efficacy and safety of colchicine for the prevention of recurrent episodes of pericarditis. Clinical and personal experience shows that colchicine may be an extremely promising adjunct to conventional treatment and may ultimately serve as the initial mode of treatment, especially in idiopathic cases.
On the basis of our reported experience with colchicine for recurrent pericarditis, we administered colchicine to two patients with large pericardial effusions complicating idiopathic pericarditis. The first was a 26-year-old male who showed clinical deterioration following emergency pericardiocentesis and aspirin (3 g/day) for 10 days; the second was a 2-year-old girl who was unsuccessfully treated with aspirin (100 mg/kg/day) for 2 weeks, followed by corticosteroids for 7 months. Administration of colchicine (1 mg/day) instead of aspirin in the first case, and with a rapid tapering-off of the corticosteroids in the second case, led to complete regression of the pericardial effusion on echocardiography within 1 week and 1 month, respectively. Colchicine was discontinued after 1 month in the first patient and was continued for 6 months in the child. Neither has had a recurrence at 24 and 6 months of follow-up, respectively. No side effects of colchicine were observed. We conclude that colchicine may be effective in the treatment of large pericardial effusion when therapy with nonsteroidal anti-inflammatory drugs and/or corticosteroids fails.
Patients with severe angina pectoris, refractory to medical treatment, in which conventional revascularization (PTCA or bypass surgery) is not possible because they present advanced coronary artery disease with a poor distal bed, account for an important clinical problem due to an increasing incidence, combined with poor quality of life, an elevated risk of severe complications, repeated hospital admissions and high mortality rate. Laser transmyocardial revascularization provides a new therapeutic alternative for these patients. Although up to now there are only a few published series, with a small number of patients, the results obtained in the two ongoing multicentric studies in Europe and the United States (including more than 500 patients at present) are quite promising. It is a simple surgical procedure, but its associated mortality is not to be dismissed (in the beginning 12% and currently 5%), because patients are in an advanced evolutionary stage. In Spain this procedure has been available since April 1996 and the results have been encouraging. In our small series we have noted a significant symptomatic improvement and better quality of life.
Clinical diagnosis of cardiac tumours is often difficult. We present the case of a 17 year-old boy in whom a left ventricular tumour was discovered during on diagnostic work-up for a syncope. The tumour was removed and histology confirmed the diagnosis of myxoma.
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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.
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.
The problem of risk stratification after myocardial infarction is reviewed. There are three major complications: new ischemic events, congestive heart failure, and malignant arrhythmias and sudden death, related to the presence of residual ischemia, left ventricular dysfunction, and electrical instability. The bidirectional interactions among these three factors is analyzed. The risk is in the middle of a triangle, the three angles of which are the above-mentioned factors. All the "satellite" factors that appear from all three angles are presented. Furthermore, the most important parameters and techniques employed to detect risk, multifactorial approach of risk stratification, and changes of risk stratification in the thrombolytic era are briefly reviewed.
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Many experimental and clinical studies have demonstrated that it is possible to trigger atrial fibrillation (AF) by vagal stimulation which reduces and disperses the atrial refractory periods and decreases the threshold of fibrillation. In order to induce fibrillation, it is necessary to deliver a stimulation near to the refractory period. It has also been shown that, in these conditions, there is a delay in atrial conduction. A temporal relationship between the preceding diastole and the coupling interval increases atrial vulnerability and plays an equally important role. The decrease in the effective atrial refractory period, especially when the values are widely dispersed, and the delay in conduction predisposing to atrial reentry, may be considered to be the two most important electrophysiological mechanisms of AF. However, in order to maintain AF, the atrium must be dilated, especially when there is a concurrent cardiac disease. The presence of a shorter "wave length" of activation allowing multiple reentry circuits is an essential condition for sustaining AF. All conductions of induction and maintenance of AF may be observed without participation of S.N.A.. When no cause of AF (atrial pathology, etc.) is apparent, a short atrial refractory period with dispersion of its values and slowing of atrial conduction in presence of an extrastimulus are the probable inducing factors.
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A randomized trial was conducted to assess the efficacy of amiodarone versus metoprolol or no antiarrhythmic treatment to suppress asymptomatic ectopic activity and improve survival in patients who have had myocardial infarction with a left ventricular ejection fraction of 20 to 45% and > or = 3 ventricular premature complexes per hour (pairs or runs). Patients (n = 368) were randomly assigned to receive amiodarone 200 mg/day (n = 115) 10 to 60 days after the acute episode, and metoprolol 100 to 200 mg/day (n = 130) or no antiarrhythmic therapy (n = 123). After a median follow-up of 2.8 years, mortality in the amiodarone-treated patients (3.5 +/- 2% SEM) did not differ significantly from that of untreated control subjects (7.7 +/- 2.5%, p = 0.19), but was lower than that in the metoprolol group (15.4 +/- 3.5%, p = 0.006). Patients treated with metoprolol had twice the mortality seen in control subjects, even though the differences were not statistically significant. Holter studies performed at 1, 6 and 12 months showed that both amiodarone and metoprolol were equally effective in reducing heart rate, whereas only amiodarone significantly reduced ectopic activity (p < 0.0001). Thus, long-term treatment with amiodarone was clearly safe in patients with an ejection fraction of 20 to 45%, was effective in suppressing arrhythmias, and was associated with a lower mortality than metoprolol; corroboration is required in a larger trial.