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Biomedical subjects

P B Oliva

Publications and source records attributed to P B Oliva.

At least 19 recordsLinked to original sources
PubMed1994

The clinical distinction between regional postinfarction pericarditis and other causes of postinfarction chest pain: ancillary observations regarding the effect of lytic therapy upon the frequency of postinfarction pericarditis, postinfarction angina, and reinfarction.

Recently two types of atypical T-wave evolution were recognized as electrocardiographic (ECG) markers of regional postinfarction pericarditis. The sensitivity and specificity of these changes for this condition were 100 and 77%, respectively. The major purpose of this investigation is to show how these ECG changes can be used to differentiate among postinfarction pericarditis, postinfarction angina, and reinfarction. Even appropriately constructed serial monitor lead ECGs can be used to make this distinction. The ease of correctly distinguishing among the three causes of postinfarction chest pain utilizing a carefully elicited history and ECG criteria is discussed. In addition, a secondary objective was to assess the effect of lytic therapy on the incidence of postinfarction pericarditis. Among the 200 patients in this study, lytic therapy halved the incidence of postinfarction pericarditis, which is in accord with the larger Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI) study.

Angina Pectoris↗
PubMed1994

T wave changes consistent with epicardial involvement in acute myocardial infarction. Observations in patients with a postinfarction pericardial effusion without clinically recognized postinfarction pericarditis.

OBJECTIVES: This study was designed to evaluate the presence or absence of atypical T wave evolution in patients with a postinfarction pericardial effusion but without clinically recognized postinfarction pericarditis. A second purpose was to evaluate the frequency of atypical T wave evolution in a previous study of postinfarction pericarditis. BACKGROUND: Electrocardiographic (ECG) criteria involving the evolution of the T wave after an acute myocardial infarction were recently described in patients with regional postinfarction pericarditis. Atypical T wave evolution was found to have a sensitivity of 100% and a specificity of 77% for clinically recognized regional postinfarction pericarditis with or without a pericardial effusion. METHODS: The hospital records and serial ECGs of 20 patients with clinically recognized postinfarction pericarditis (Group I) were reviewed. The records and serial ECGs of 20 additional patients with a postinfarction pericardial effusion without clinically recognized postinfarction pericarditis (Group II) were also examined. The type of postinfarction T wave pattern, typical or atypical, was recorded in both groups. RESULTS: All 20 patients in Group I had atypical T wave evolution. Among the 20 patients in Group II, every patient also had atypical T wave evolution. Fifteen percent of all 40 patients with atypical T wave evolution had a non-Q wave infarction with definite or inferred postinfarction pericarditis. CONCLUSIONS: The high sensitivity of atypical T wave evolution in diagnosing regional postinfarction pericarditis was confirmed. However, similar T wave alterations were also observed when a postinfarction pericardial effusion existed in the absence of clinically recognized pericarditis. Fifteen percent of patients with atypical T wave evolution had a non-Q wave infarction with definite or inferred pericardial involvement. Thus, the presence of atypical T wave evolution may be a more sensitive indicator of a transmural infarction than the development of a Q wave.

Electrocardiography↗
PubMed1993

Cardiac rupture, a clinically predictable complication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations.

OBJECTIVE: To test the hypothesis that certain clinical events may precede free wall myocardial rupture and allow its prediction, we conducted a retrospective and prospective study of 70 patients with rupture. BACKGROUND: Rupture of the left ventricular free wall develops in approximately 10% of patients with fatal acute transmural myocardial infarction. Clinically, its occurrence has been considered precipitous and unexpected. Pathologically, however, rupture appears to be a stuttering, progressive process characterized in many instances by an infiltrating intramural hemorrhage and a thrombus within the tear of > or = 1 day's duration. METHODS: The clinical course and evolutionary electrocardiographic (ECG) changes in 70 consecutive patients with rupture and 100 comparison patients with acute myocardial infarction but without rupture were reviewed to ascertain whether certain clinical symptoms, signs and ECG alterations occur in patients prone to develop rupture, allowing its anticipation. In addition, a correlation was established between the site of infarction indicated by the ECG and the site of rupture determined at autopsy or surgery. RESULTS: Patients with rupture had a significantly greater incidence of pericarditis, repetitive emesis and restlessness and agitation than did patients without rupture. More than 80% of patients with rupture had two or more symptoms compared with 3% of patients without rupture (p < 0.002). A deviation from the expected evolutionary T wave pattern occurred in 94% of patients with rupture and 34% of control patients (p < or = 0.02). An abrupt transient episode of hypotension and bradycardia, probably due to the initial tearing of the epicardium with a resultant small hemopericardium, was observed in 21% of patients with rupture. Rupture of the midlateral wall was most common (32%) and usually occurred in the setting of an inferoposterolateral infarction related to an acute left circumflex artery occlusion. On the basis of these clinical and ECG changes, rupture was confirmed by echocardiography and pericardiocentesis in the two most recent patients, and the defect was successfully repaired. CONCLUSIONS: Rupture is often preceded by particular symptoms, signs--namely, one or more episodes of abrupt, transient hypotension and bradycardia and unexpected alterations of the T waves, especially directional changes of the latter. Patients displaying these symptoms, signs and ECG changes require a bedside echocardiogram and echocardiographically guided pericardiocentesis if fluid is visualized. If the pericardiocentesis identifies the fluid as blood, immediate surgery is indicated.

Aged↗
PubMed1993

The electrocardiographic diagnosis of regional pericarditis in acute inferior myocardial infarction.

The diagnosis of postinfarction localized (regional) pericarditis has remained elusive. During the course of a recent study of patients with fatal free-wall rupture, an atypical pattern of T-wave evolution was observed during the days preceding death. It was learned, from autopsy examination, that these electrocardiographic changes were due to the associated localized pericarditis, rather than the rupture, per se. Therefore, this investigation was undertaken to ascertain if the same atypical T-wave changes occur in patients with postinfarction localized pericarditis, but without free-wall rupture, and to determine if the frequency of those changes differs between those patients with inferior and those with anterior postinfarction pericarditis. Forty-three patients with regional postinfarction pericarditis were identified clinically. They were divided into three groups, anterior (17), inferior (17) and lateral or posterior (9) myocardial infarction. In this report those patients with anterior regional postinfarction pericarditis are compared with those with inferior postinfarction pericarditis. It was found that an atypical T-wave evolution pattern--either persistently positive T-waves after 48 h or reversal of initially inverted T-waves after 48 h--existed in every patient irrespective of infarct location. However, the two atypical patterns of T-wave evolution occurred with distinctly different frequencies between the two sites of infarction. With inferior postinfarction pericarditis, gradual reversal of initially inverted T-waves occurred in 14 patients (82%) while only three (18%) had persistently positive T-waves. Conversely, among patients with anterior postinfarction pericarditis, reversal after inversion occurred in five of 17 patients (29%) while 12 of 17 patients (71%) had persistently positive deflections (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Electrocardiography↗
PubMed1993

Electrocardiographic diagnosis of postinfarction regional pericarditis. Ancillary observations regarding the effect of reperfusion on the rapidity and amplitude of T wave inversion after acute myocardial infarction.

BACKGROUND: The ECG recognition of diffuse pericarditis following acute myocardial infarction has been based on changes of the ST segment and, to a lesser extent, alterations of the PQ segment. No ECG criteria exist for the diagnosis of postinfarction regional pericarditis. Recently, it was observed that the T wave evolution follows an atypical pattern before fatal free wall rupture and that this pattern is due to the associated pericarditis. Therefore, this study was conducted on 200 patients with acute myocardial infarction to further elucidate the sensitivity and specificity of the atypical T wave changes in patients with regional postinfarction pericarditis without rupture and to assess the affect of lytic treatment on the rapidity and amplitude of postinfarction T wave evolution. METHODS AND RESULTS: An analysis of the clinical courses and serial ECGs of 200 consecutive patients with acute myocardial infarction was performed. Among 43 patients with postinfarction pericarditis, the pattern of T wave evolution consistently differed from the customary postinfarction pattern of T wave evolution. This unusual evolutionary course was expressed as either persistently positive T waves 48 or more hours after infarction (67%) or premature, gradual reversal of inverted T waves to positive deflections (33%). The sensitivity and specificity of these T wave alterations were 100% and 77%, respectively. The only other processes identified that caused this type of postinfarction T wave evolution were cardiopulmonary resuscitation, reinfarction, and very small infarcts. Both reperfusion, as judged by the creatine kinase-MB curve, and patency, as assessed by the angiogram, were correlated with the rapidity and depth of T wave inversion. Ninety percent of patients with reperfusion attained a maximum T wave negativity of 3 mm or more within 48 hours after the onset of chest pain in the lead that initially displayed the greatest ST segment elevation. Seventy-six percent of patients without reperfusion attained a maximum negativity of 2 mm or less within 72 hours. Thus, like the ST segment, accelerated evolution and deepening of the T wave may be noninvasive markers of reperfusion. CONCLUSIONS: First, premature reconcordancy of the ST segment and T wave after acute myocardial infarction is a sensitive, reasonably specific, and easily recognizable ECG manifestation of postinfarction regional pericarditis. Second, reperfusion is associated with accelerated evolution and deepening of the T waves following acute myocardial infarction.

Clinical Enzyme Tests↗
PubMed1984

Unstable rest angina with ST-segment depression. Pathophysiologic considerations and therapeutic implications.

Because of recent findings, a reassessment is needed of the concept that rest angina associated with ST-segment depression is due to a spontaneous, transient increase of blood pressure or heart rate, or both, in the presence of critical coronary artery stenosis. Continuous hemodynamic and electrocardiographic recordings done before and during attacks of rest angina and thallium-201 scintigrams done during pain indicate that a transient reduction of flow is the immediate cause of ischemia in most, but not all, instances. Flow reduction, in turn, appears to be due to coronary arterial spasm or platelet aggregation, or both, acting at a site of atherosclerotic narrowing. Therapy for unstable rest angina should include measures to prevent both transient reductions of flow and increases of myocardial oxygen consumption. A combination of long-acting nitrates, a beta-blocker, a calcium-channel blocker, and aspirin or heparin is suggested for this purpose. Intravenous nitroglycerin is useful when angina occurs despite this therapy or when frequent attacks of ischemia are occurring at the time of admission.

Angina Pectoris↗
PubMed1983

The role of alcohol in new-onset atrial fibrillation.

Forty cases of new-onset atrial fibrillation (AF) were reviewed to establish the frequency of various causes. Alcohol intoxication caused or contributed to 14 cases (35%). Coronary artery disease (22.5%) and pulmonary disease (22.5%) were also common causes of acute AF. Among patients less than 65 years old, alcohol caused or contributed to approximately two thirds (63%) of the cases of AF. Thyrotoxicosis was uncommon (one case in 40); no patient had a diagnosis of mitral stenosis, pulmonary embolism, or pericarditis. There were no complications of AF in alcoholic patients; the majority (88.9%) converted spontaneously to a normal sinus rhythm within 24 hours. Alcohol intoxication should be considered early in the differential diagnosis of new-onset AF in young patients. Many patients may not require admission to an intensive care unit or a costly battery of diagnostic tests.

Aged↗
PubMed1981

Pathophysiology of acute myocardial infarction, 1981.

Recent observations and discoveries necessitate reassessing the pathophysiology of acute myocardial infarction. Platelet aggregability has been shown to be increased in patients with an acute myocardial infarction, and coronary arterial spasm has been documented by arteriography done just before and during the onset of infarction. These clinical observations have been complemented by the recent discovery of two potent substances; thromboxane A2 and prostacyclin, which affect platelet aggregability and coronary arterial tone. These recent observations and discoveries are blended with older pathologic information to attain a more comprehensive understanding of the pathophysiology of acute myocardial infarction. A dynamic interaction among damaged intima, platelet aggregates, and spasm is postulated to occur as a prelude to thrombosis in acute transmural myocardial infarction. Spasm appears to initiate the infarction process in some instances, but the exact sequence of events has not been established.

Aged↗
PubMed1979

Quality of survival after out-of-hospital cardiac arrest: predictive value of early neurologic evaluation.

One hundred and seventeen patients were admitted following out-of-hospital cardiac arrest. After initial neurologic evaluation, they were followed prospectively until discharge or death. Seventeen patients were alert when admitted. Of these, four died and 10 of 13 survivors were neurologically normal. One hundred of the patients were unresponsive; of these, 60 died. Of 40 survivors, 15 were neurologically normal, at discharge; 15 could perform some self-care but were confused, and 10 required total care. Absence of pupillary light reaction, oculocephalic reflexes, purposeful response to pain, and spontaneous respirations were associated with high mortality and more severe neurologic deficits. However, some patients with usually unfavorable signs recovered good neurologic function.

Aged↗
PubMed1979

Obstruction of the proximal right coronary artery with acute inferior infarction due to blunt chest trauma.

Two patients developed an acute transmural myocardial infarction due to severe obstruction of the proximal right coronary artery after blunt chest trauma. Neither had a history of ischemic heart disease, and both had an arteriographically normal left coronary artery. In one patient significant resolution of the subtotal obstruction occurred within 3 months. An intimal tear or subintimal hemorrhage with luminal thrombosis, or both, are the suggested mechanism of coronary arterial occlusion. Spasm and platelet aggregates may contribute. Despite a large number of automobile accidents, obstruction of the right coronary artery due to blunt chest trauma has not been previously described. This suggests it has been overlooked and should be especially suspected in persons with injury to the sternum and an acute inferior myocardial infarction.

Accidents, Traffic↗