P-wave analysis in myocardial infarction,pulmonary edema,and embolism

In a retrospective study, the P-terminal force in Lead V₁ (PTF-V₁) was measured in three groups, each of 35 patients, with the respective diagnoses of acute myocardial infarction without pulmonary edema, acute pulmonary embolism, and acute pulmonary edema. In all but one of the patients with acute pulmonary edema, a highly negative PTF-V₁ value was obtained, whereas by contrast, all the patients with pulmonary embolism had normal PTF-V₁ values. Four of the patients with acute myocardial infarction had abnormal PTF-V₁ values, although at the time there was no clinical or radiologic evidence of pulmonary edema. However, one of these patients did develop acute pulmonary edema a few hours later.Measurement of the PTF-V₁ is a simple noninvasive test that may, therefore, be useful in separating patients with acute pulmonary embolism from those with acute or impending pulmonary edema.     

Aspirin, hyperventilation, and cerebellar infarction in sickle cell disease

Aspirin ingestion was followed by hyperventilation, cerebellar signs, and fatal brain stem dysfunction in a patient with sickle cell disease. Autopsy showed a swollen, recently infarcted cerebellum with tonsillar herniation compressing the medulla. We propose that hypocapnea from aspirin-induced hyperventilation caused carotid artery constriction and focal cerebral hypoxia, resulting in cerebellar sickling nad infarction. Hypocapnea should be treated promptly to prevent brain damage in patients with sickle cell disease.     

Acute infarction,intracoronary thrombolysis,and primary PTCA in pregnancy

Acute myocardial infarction has an incidence in pregnancy of 1 in 10,000, with a mortality ranging from 37–50%. Mortality is increased if the infarct occurs in the third trimester, if the patient is under age 35 yr, if she delivers within 2 wk of her infarct, and if she has a cesarean section. We present a case involving all four prognostically poor factors. The patient was treated emergently in the cardiac catheterization laboratory with intracoronary thrombolysis and primary PTCA of an occluded LAD. She had an uncomplicated recovery and subsequent delivery of a healthy child with no peripartum cardiac complications. A review of myocardial infarction in pregnancy follows. Cathet. Cardiovasc. Diagn. 42:38–43, 1997. © 1997 Wiley-Liss, Inc.     

An elderly patients with ventricular aneurysm, thrombus in the aneurysm, and cerebral infarction 10 years after myocardial infarction]

A 75-year-old man had a 26-year history of hypertension and an 18-year history of effort angina pectoris. He suffered acute myocardial infarction at age 61. According to serial echocardiography, the initially hypokinetic segment of the left ventricular apex was transformed to an apical aneurysm over the course of 10 years (at age 71). Ten months later, a transient ischemic attack occurred, despite the administration of aspirin. At age 72, echocardiography revealed a hyperechoic lesion that was suspected to be a thrombus within the aneurysmal cavity. Cerebral infarction (right occipital lobe) occurred 13 years after myocardial infarction, at age 73. After warfarin therapy for 3 months, the thrombus-like echo in the left ventricular aneurysm disappeared.     

Helicoid ventricular tachycardia, torsade de pointes, in acute myocardial infarction

Helicoidal ventricular tachycardia (Torsades de Pointe), (HVT) is an arrhythmia with peculiar characteristics and therefore should be individualized. The occurrence of HVT during acute myocardial evolution has been denied by many authors. In this paper, the possibility that this association may be not only coincidental is analyzed. A group of 1,307 patients with acute myocardial infarction was studied, in 29 of them this arrhythmia was detected in the first 72 hours and these patients didn't have an associated disease and/or treatment related to HVT. This represents an incidence of 2.22% in this group. The helicoidal ventricular tachycardia had a peculiar behavior, different to the one found in HVT of other etiologies. It was triggered by early premature ventricular beats, it was found even in cases with supraventricular tachycardia and acute atrio--ventricular heart block, very seldom is autolimited and usually degenerates into ventricular fibrillation, the most important factor in association with this arrhythmia is QT prolongation. Intracavitary pacing is the treatment of choice.     

Non-Q wave myocardial infarction. Recurrent myocardial infarction, unstable angina and arrhythmia in 8-year observation

The contradictory views on long term clinical course of patients after non-Q wave myocardial infarction (NQMI) as compared with those after Q wave myocardial infarction (QMI)--induced us to undertake a comparative study of both types of myocardial infarction during a 8 year follow-up. The study was carried out in 400 patients (pts) with NQMI (mean age 51) and 485 pts with QMI (mean age 53). Both groups were compared. We have analysed the following parameters: the dynamics of ischaemic heart disease (unstable angina, reinfarction, arrhythmias, mortality) and coronary arteriography. During 8 year observation unstable angina and arrhythmias, were statistically more frequent in pts after NQMI. Recurrent myocardial infarction occurred in 196 (49%) of pts after NQMI and only in 87 pts (18%) after QMI (p less than 0.001). However, the difference in mortality between both groups was not significant (37% vs 39% respectively). Coronary angiography was performed at 1-6 months after myocardial infarction. In 65% of pts after NQMI detected lesions were limited to proximal part of one or two coronary arteries. Conclusion: NQMI is characterized by unstable long-term clinical course, and that is why pts with NQMI should be recommended for early coronary angiography and revascularization.     

Apoptosis in myocardial ischemia, infarction, and altered myocardial states.

The work ahead necessary to develop and refine clinically useful antiapoptotic therapy in ischemic-reperfusion injury is daunting. There are many unanswered questions. What is the best method of detecting apoptosis in the cardiac myocytes? What will be the most practical method to deliver this therapy to the cardiac myocyte? Will antiapoptotic agents act selectively on affected myocytes to provide clinical efficacy? Will antiapoptotic agents be effective, or will they be limited by dose heterogeneity? If antiapoptotic is proven to have long lasting efficacy, should it be used for all patients with myocardial infarction or confined only to patients with left ventricular dysfunction. Will antiapoptotic therapy be so effective that it replaces ACE inhibitors and betablockers, or will it always be used as an adjunct to an ACE inhibitor or a betablocker? These questions lay the foundation for investigation for the next decade.