Incidence and complexity of ventricular ectopy during Holter monitoring in patients with exercise-induced myocardial ischemia and normal or mildly reduced left ventricular function.

We aimed to assess the relationship between frequent and complex ventricular ectopy by continuous electrocardigraphic 24-hours Holter monitoring in patients with coronary artery disease and inducible ischemia during exercise procedures. We investigated 609 consecutive patients. They were referred for chest pain (28% with a previous myocardial infarction, older than 6 months). In all population patients radionuclide ventriculography showed a global normal or mildly reduced left ventricular function (ejection fraction > 45%). All patients showed exercise-induced myocardial ischemia (ST depression) and exercise thallium-201 reversible defects. During Holter monitoring, in study population, divided according to incidence of premature ventricular complexes (PVC), we found a higher prevalence of complex ventricular arrhythmias (CVA) (bigeminy, couplets, ventricular tachycardia, multiformity) in patients with high incidence of PVC. The relationship between frequent and complex ventricular ectopy has been observed also during ischemic ST shifts occuring during 24-hours monitoring. In contrast, the R on T phenomenon was not related to incidence of PVC. Therefore, in patients with exercise-induced myocardial ischemia and global normal or mildly reduced left ventricular function there is a relationship between frequent and complex ventricular ectopy, as previously suggested in CAD patients with depressed left ventricular function.

Different protocols generate variations in systolic blood pressure response after exercise in patients with coronary artery disease.

Some patients with coronary artery disease (CAD) and exercise-induced myocardial ischemia demonstrate no change or a paradoxical increase in systolic blood pressure (SBP) during recovery following exercise. Previous studies have investigated the significance and clinical usefulness of analysis of recovery SBP response in detecting CAD, but conflicting data have been reported. Different protocols were used for the time of SBP recording and either bicycle or treadmill testing. We studied the exercise response in 64 male patients investigated for CAD who underwent symptom-limited treadmill stress testing during electrocardiographic monitoring and serial recording of blood pressure. Forty-three patients showed on or more stenoses of at least 70% at angiography (CAD). Twenty-one patients with normal coronary tree or slight lesions served as controls. The sensitivity (true positive/all CAD patients), specificity (true negative/all CAD-free patients), and the correct classification rate (correct diagnoses/all subjects) were assessed by standard ST segment analysis and two recovery SBP ratios calculated by dividing the first minute recovery SBP by the immediate postexercise value (RR/R) or by the true peak exercise value (RR/P). ST segment analysis achieved 53% sensitivity, 57% specificity, and 54% correct classification, the RR/R ratio achieved 73%,23%, and 60%, and the RR/P ratio 53%, 71%, and 59%, respectively. There were significant differences in results using these ratios. Time of SBP recording generated discrepancies in recovery SBP ratios. Therefore, differences in the timing of SBP measurement may generate conflicting clinical indications.

Clinical, controlled trial of somatostatin with ranitidine and placebo in the control of peptic hemorrhage of the upper gastrointestinal tract.

There are many controversies concerning the treatment of hemorrhages of the upper gastrointestinal tract. In order to determine whether some currently used drugs, such as somatostatin (SST) and ranitidine, may be useful in the control of hemorrhages, we have conducted a controlled (not blind) study with alternate assignment in 220 accurately selected patients affected with hemorrhage secondary to acute peptic ulcer disease. We divided the patients into three groups on the basis of the severity of disease (moderate, serious, massive); a subgroup of each group underwent one of the three studied treatments (SST, ranitidine, placebo). After careful clinical and laboratory assessment, we followed the patients over a period of 72 h. The criteria to assess the efficacy of the treatment were: number of patients who had stopped bleeding; time needed to stop the hemorrhage, and the number of recurrences of bleeding in every group and subgroup. At the end of the study, SST and ranitidine were more effective in the control of hemorrhage than placebo. SST was more effective than ranitidine, especially in patients with moderate and serious hemorrhages; it achieved a recovery of nearly 100% in the group with moderate bleeding.

A myeloma paraprotein with specificity for platelet glycoprotein IIIa in a patient with a fatal bleeding disorder.

Impaired platelet aggregation, normal shape change, and agglutination and normal ATP secretion and thromboxane synthesis in response to high concentrations of thrombin or arachidonic acid were found in a patient with multiple myeloma and hemorrhagic tendency. The purified IgG1 kappa or its F(ab1)2 fragments induced similar changes when added in vitro to platelet-rich plasma from normal subjects. In addition, the paraprotein inhibited adhesion to glass microbeads, fibrin clot retraction, and binding of radiolabeled fibrinogen or von Willebrand factor to platelets exposed to thrombin or arachidonic acid without affecting intraplatelet levels of cAMP. The radiolabeled para-protein bound to an average of 35,000 sites on normal platelets but it bound to less than 2,000 sites on the platelets from a patient with Glanzmann's thrombasthenia. Immunoprecipitation studies showed that the platelet antigen identified by the paraprotein was the glycoprotein IIIa. Furthermore, binding of radiolabeled prostaglandin E1 (PGE1) to resting platelets as well as binding of von Willebrand factor to platelets stimulated with ristocetin were entirely normal in the presence of patient's inhibitor. These studies indicate that bleeding occurring in dysproteinemia may be the result of a specific interaction of monoclonal paraproteins with platelets. In addition, our data support the concept that the interaction of fibrinogen and/or von Willebrand factor with the platelet glycoprotein IIb-IIIa complex is essential for effective hemostasis.