Ignacio Cruz

[Kinetics of C-reactive protein release in different forms of acute coronary syndrome].

INTRODUCTION AND OBJECTIVES Better knowledge of C-reactive protein (CRP) kinetics could lead to improved clinical application of this biomarker. METHODS We studied 110 patients: 42 had ST-elevation acute myocardial infarction (STEMI), 35 had non-ST-elevation acute myocardial infarction (NSTEMI), and 33 had unstable angina. Patients were admitted to our institution within 6 hours of symptom onset. The levels of CRP, troponin-I, and creatine kinase MB fraction (CK-MB) were measured on admission and every 6 hours during the first 48 h. The CRP level was also measured daily until hospital discharge. RESULTS The median (interquartile range) CRP level increased relative to baseline from 6 hours after admission, from 5 (2-9) mg/L to 6 (3-10) mg/L (P=.004). Although, CRP levels on admission were similar in all groups, there was a significant difference in peak CRP level: it was 67 (36-112) mg/L in the STEMI group, 29 (20-87) mg/L in the NSTEMI group, and 18 (12-36) mg/L in the unstable angina group. The maximum CRP level was observed 49 (38-53) hours after the onset of symptoms, but occurred later in patients with STEMI. Although there was only a weak non-significant correlation between CRP and troponin levels (r=0.135) at admission, the maximum CRP level was found to be influenced by the degree of myocardial damage (r=0.496; P< .001). CONCLUSIONS The pattern of CRP release observed was clearly different in different forms of acute coronary syndrome. Although the CRP level measured at admission was similar in all patient groups, it was influenced by the degree of early myocardial tissue necrosis. This variation in CRP kinetics should be taken into consideration when designing future studies.

Recurrent Coronary Thrombosis, Factor V Leiden, Primary Antiphospholipid Syndrome, and HIV

We describe a 54-year-old man who was HIV-positive, admitted for cardiogenic shock complications inferior myocardial infarction. He was treated with primary percutaneous transluminal angioplasty (PCTA) and stent deployment in mid right coronary artery. After a few days thrombotic occlusion of the stent occurred, and the problem recurred during implantation of a new stent in the course of a second PTCA. We detected coinheritance of factor V Leiden, primary antiphospholipid syndrome and antithrombin deficiency. We discuss the role of these coagulation disorders in acute myocardial infarction as well as the treatment and course of the coronary syndrome in this context.

Trombosis coronaria recurrente, síndrome antifosfolipídico primario, factor V Leiden y virus de la inmunodeficiencia humana

Presentamos el caso de un varon de 54 anos, positivo frente al virus de la inmunodeficiencia humana, que ingresa por un infarto agudo de miocardio inferior en shock cardiogenico. Se realiza una angioplastia primaria con implantacion de stent en la arteria coronaria derecha media. A los pocos dias presenta una oclusion trombotica del stent recien implantado; incluso durante la nueva angioplastia coronaria transluminal percutanea (ACTP)- stent se produjo una segunda oclusion intraoperatoria. Se constato la presencia de factor V Leiden, sindrome antifosfolipidico primario y deficit de antitrombina III. Se expone el papel de estos trastornos de la coagulacion en el infarto agudo de miocardio, asi como el tratamiento y la evolucion del sindrome coronario en este contexto.

Relationship between C-Reactive Protein and the Electrocardiographic Pattern on Admission in Patients with Acute Coronary Syndrome

Background: In patients with acute coronary syndrome (ACS), the prevalence of a primary inflammatory pathogenic component of coronary instability, as detectable by elevated C-reactive protein (CRP), varies considerably. The aim of the present study was to assess the prevalence of inflammation in patients with ACS according to the different electrocardiographic (ECG) patterns on admission. Methods: Hundred and thirty-six consecutive patients with the diagnosis of acute myocardial infarction were divided in three groups according to the ECG pattern on admission. Group 1 included 59 patients with ST segment elevation, group 2 included 50 patients with ST depression and/or T wave inversion and group 3 included 27 patients with no ECG changes. CRP was measured on admission in all patients. For the prevalence of inflammation analysis, we used a cutoff value of 3 mg/l. Results: CRP was above cutpoint significantly more often in patients with ST depression and/or T wave inversion (44.1% in group 1, 70% in group 2 and 40.7% in group 3; p = 0.009). Patients with similar ECG pattern and CRP levels above the cutpoint presented a poorer outcome (coronary death, myocardial infarction and recurrence of instability) at one-year follow-up: 54 versus 27% for group 1, 74 versus 27% for group 2 and 45 versus 31% for group 3. Conclusions: Patients with ST depression and/or T wave inversion on admission exhibit a higher prevalence of elevated CRP than those with ST elevation or no ECG changes, suggesting an important heterogeneity of the role of inflammatory triggers of the clinical syndromes of coronary instability.

Unusual Electrocardiographic Presentation of Arrhythmogenic Right Ventricular Cardiomyopathy

Arrhythmogenic right ventricular cardiomyopathy or dysplasia (ARVD) is a genetically determined heart muscle disease in which the myocardium is replaced by fibroadipose tissue. It is associated with arrhythmias, heart failure and sudden death.1 Typical symptoms include palpitations, dizziness and syncope. Sudden death is often the first sign, especially in young people, and it coincides with some type of strenuous physical activity; in some series, it accounts for up to 20% of all sudden deaths in young adults.2 With the introduction of automatic implantable defibrillators, many of these deaths can be prevented. However, the prevention of arrhythmic death requires timely diagnosis, which depends on the ability of the primary care physician and the specialist to be aware of and to diagnose this disease. The diagnosis is established on the basis of certain major and minor criteria involving the evaluation of the family history, the depolarization or repolarization-induced electrocardiographic changes, arrhythmias, structural changes and ventricular dysfunction, and on the histopathological features.3 At the present time, there are a number of registries underway for the purpose of analyzing the validity of these criteria and broadening them, if appropriate.4 The typical clinical signs, together with T-wave inversion in leads V1 to V3 present in over 50% of the patients,5 or the appearance of the epsilon wave in 30%,6 raise the suspicion of this disease; however, there are reports of cases in which the electrocardiographic features were less common, but the risk of sudden death was the same.7 We present the case of a 31-year-old man, a professional soccer player, who was referred to our unit because of occasional palpitations. After initial evaluation and the verification of the absence of a family history of heart disease, we examined the electrocardiogram, which revealed negative T waves in leads II, III, and aVF and ventricular premature beats with right bundle branch block (RBBB) morphology (Figure 1). During 24-hour Holter monitoring, several episodes of nonsustained ventricular tachycardia (NSVT) were recorded, as were premature beats with RBBB morphology that appeared to originate in the left ventricular apex. Transthoracic echocardiography revealed a slightly dilated left ventricle with apical akinesia. Given these findings, the patient underwent single photon emission computed tomography (SPECT) to study myocardial work, reaching 20 MET without symptoms, but with frequent premature beats and self-limited episodes of NSVT similar to those recorded during 24-hour Holter monitoring. The scintigraphic images disclosed a fixed apical perfusion defect. In view of these findings, coronary arteriography was carried out, but no lesion of any type was observed; however, ventriculography revealed the presence of left ventricular apical akinesia. Right ventricle was dilated and unstructured, with akinetic/dyskinetic areas and diastolic septal bulge (“stack of coins”; Figure 2). As ARVD was suspected, magnetic resonance imaging was requested. It revealed fatty infiltration of the right ventricle. ARVD with involvement of the left ventricle was diagnosed.

Combined Percutaneous Mitral Valve Implantation and Paravalvular Leak Closure in a High-risk Patient With Severe Mitral Regurgitation

evidence thus indicates that women at very high or high CVR receive less effective treatment than men in the same risk categories. Our study highlights the value of research into strategies aimed at increasing health care professionals’ awareness of the need for gender equality in the approach to CVR, especially in relation to women in secondary prevention or at very high or high risk. This would also result in a more efficient use of lipid-lowering drugs.