Desencadenantes de síndromes coronarios agudos. Relaciones fisiopatológicas / Triggering of acute coronary syndromes. Pathophysiologic relationships

In this review, the relationship of external triggers with the development of acute coronary syndromes is described. Based on current evidence, the pathophysiological mechanisms that probably result in the rupture of vulnerable coronary plaques are revised and preventive measures to stop the functional and lethal consequences of its occurrence are proposed.

[The P wave in systemic arterial hypertension. Comparison with the echocardiogram and apexcardiogram]. / La onda P en la hipertensión arterial sistémica. Correlación con el ecocardiograma y el apexcardiograma.

The cause of an abnormal electrocardiographic P wave (AEPW) in systemic arterial hypertension (SAH) has not been delucidated. In order to demonstrate if this sign is related to volume overload of the left atrial cavity -previously we found no correlation between pressure overload of the cavity and the presence of an AEPW- 34 patients with SAH were studied; population were divided in two groups: group A (GA, n = 13), formed by 13 cases with a P wave more than 0.10 s duration (D2 standard lead) and group B integrated by 21 cases with a P wave at 0.10 s or less duration. In each cases phonocardiographic and echocardiographic (Mode M) studies were performed and the following data were obtained: "A" index (AI), left atrial dimension (LAD) and, septal (SD) and left posterior wall dimension (LPWD); besides: Sokolow electrocardiographic index (SI) and systolic (SBP) and diastolic (DBP) blood pressure. Results are shown in the following table: (Table: see text). There were not statistical differences between groups (data of SBP and DBP not shown). Correlation between LAD and AI and duration of P wave were not statistical different (data not shown). An AEPW in SAH does not seem to be cause by a volume left atrial overload. Possible it is related to an interatrial conduction defect.

[The P-wave in systemic arterial hypertension]. / La onda P en la hipertensión arterial sistémica.

An abnormal electrocardiographic P wave (AEPW) has been interpreted as indicative of heart failure, hypertrophy or dilatation of left atrium, or diminished left ventricular compliance. In order to determine the significance of this electrocardiographic sign we studied 47 cases of systemic arterial hypertension (SAH) without heart failure or coronary obstruction. Patients were assigned at 2 groups: group A (22 cases with P wave duration greater than 0.11 seg. (LEAD D2); and group B 25 cases with P wave duration less than this. The following data were studied in all cases: left ventricular ejection fraction (LVEF), left ventricular presystolic filling fraction (LVPFF), Sokoloff electrocardiographic index (SEI), final diastolic pressure of LV (FDPLV), and systolic arterial pressure (SAP). Results were: (Table: see text). There were not statistical differences in these values between groups A and B (including the FDPLV value not shown in the table). Correlation coefficient between duration of P wave and the other parameters studied were also no significant. AEPW in SAH is not related to an specifically degree of left ventricular hypertrophy or disfunction; therefore, hypertensive heart disease should not be classified taking in account this electrocardiographic sign.

The role of surface charge and hydrophobic interaction in the activation of rat liver adenylate cyclase.

Rat liver plasma membranes were incubated either with procaine, lidocaine or tetracaine to study the binding of glucagon to receptors and the responses of adenylate cyclase to glucagon or fluoride. Procaine treatment increased the glucagon and fluoride activation of the cyclase and the stimulation was concentration-dependent; this compound seemed to act at the G/F unit level since changes in the glucagon binding were not observed and the basal activity was not modified. Tetracaine inhibited the adenylate cyclase activity in the order glucagon greater than basal greater than fluoride; it seems that tetracaine acted at the receptor unit level since it reduced the binding affinity. Tetracaine at high concentration (10 mM) also inhibited the fluoride stimulation of the Lubrol PX-solubilized enzyme; apparently the anesthetic acts on the G/F unit and this would indicate the component is still bound to the catalytic unit. The solubilized enzyme is not longer stimulated by procaine. These data suggested that the F component site of the G/F units is in some aspects different to the G component and more resistant to the detergent. The results of this work allowed a clear distinction among the different components of the glucagon-stimulated adenylate cyclase system and showed the importance of surface charge and hydrophobic interactions as regulatory mechanisms.