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Biomedical subjects

C R Conti

Publications and source records attributed to C R Conti.

At least 217 records · Page 12Linked to original sources
PubMed1989

Unstable angina pectoris: pathogenesis and management.

Unstable angina is a simple term used to describe a complex group of conditions with a heterogeneous pathogenesis and prognosis. In patients with cardiac disease, understanding pathogenetic mechanisms often influences decisions regarding prognosis and treatment. Potential causes for the development of acute myocardial ischemia include: 1. Extracardiac factors in the patient with severe coronary atherosclerosis. 2. Plaque disruption resulting in: a. Transient platelet aggregation in diseased vessels. b. Dynamic or intermittent coronary artery thrombosis. c. Hemorrhagic dissection into an atheromatous plaque. d. Abnormal constriction of a coronary artery. 3. Progression of atherosclerosis as a result of plaque "healing." It may not be possible to identify the appropriate mechanism responsible for unstable angina in every case but the clinician must attempt to do so since the selection of appropriate therapy for the individual patient depends on the mechanisms responsible for the symptoms.

Angina Pectoris↗
PubMed1989

Conventional drug therapy of patients with acute myocardial infarction.

In medicine and in cardiology one must be aware that there is no "standard" management for any condition. However, some guidelines can be offered for the management of myocardial infarction in the early stages. The following can be considered an aggressive but stepwise approach to therapy of patients with suspected myocardial infarction using conventional drugs with or without thrombolytic therapy or coronary angioplasty. Any patient presenting with prolonged chest pain occurring at rest should have an electrocardiogram. If the ECG is abnormal, an evolving myocardial infarction can be suspected. In this setting, oxygen should be administered if the patient is dyspneic, cyanotic, or has rales in the chest, intravenous nitroglycerin should be given, and the patient's response should be assessed. Caution should be observed at this point if the patient is sweating or hypotensive. Administration of a vasodilator in a dehydrated patient may drop the blood pressure further. If pain is relieved and the ECG returns to normal, the working diagnosis is severe angina. However, acute myocardial infarction should not be dismissed. A strong case for the use of intravenous heparin can be made to prevent the redevelopment of intracoronary clot inasmuch as thrombosis probably occurs in most patients presenting with unstable and severe angina, as it most surely does in patients with an evolving acute myocardial infarction. If nitrates and oxygen relieve chest pain but the ECG remains abnormal, for example, ST segment elevation, the diagnosis of acute evolving myocardial infarction must be considered and intravenous nitrates should be continued. If the patient has no relief of pain from nitrates and oxygen and the ECG remains abnormal, morphine sulfate should be administered intravenously in sufficient dosage to relieve the chest pain but not produce hypotension or hypoventilation. Once the diagnosis of myocardial infarction has been made, some would begin administering intravenous lidocaine as prophylaxis against the ventricular arrhythmias commonly encountered in the earlier stages of myocardial infarction. It has not been my practice to use prophylactic lidocaine, but I believe it is prudent to have a low threshold for the use of this drug in patients with frequent PVCs, especially if they are multifocal. If the patient exhibits symptomatic bradycardia or heart block, a trial with intravenous atropine is warranted. Additionally, while all of this is going on, one should contemplate using beta-blockers if there is good indication, and thrombolytic therapy if there are no contraindications to its use.

Cardiovascular Agents↗
PubMed1989

Early postinfarction angina: therapeutic strategies.

In patients with recurrent chest pain in the immediate postinfarction state, one must determine whether the recurrent chest discomfort is related to myocardial ischemia or not. If recurrent ischemia is present then it may be due to either (1) transient increase of myocardial oxygen demand over a fixed coronary reserve, (2) transient decrease of myocardial oxygen supply, or (3) a combination of both. Coronary angiography reveals that most patients have double or triple vessel disease. The presence of postinfarction angina portends a poor prognosis. Reinfarction rate has been reported as high as 28% during initial hospitalization and mortality has been as high as 57% at six months follow-up. Intravenous nitroglycerin seems to be an important foundation therapy for the management of postinfarction angina. The use of beta blockers has reduced mortality by 24% compared to placebo in this patient subgroup. Calcium antagonists have proven efficacious in patients with non-Q-wave myocardial infarction and postinfarction angina. Thrombolytic therapy, chronic anticoagulation and antiplatelet therapy are not proven efficacious at this time. Coronary angioplasty is usually successful initially but is associated with an early myocardial infarction rate varying from 1.4 to 13%. Mortality rate is usually low as is late myocardial infarction rate. Recurrent angina occurs commonly in these patients. Surgical therapy in the early infarction state should be offered to those patients who have a poor response to maximal medical therapy whose coronary artery obstructions are not amenable to PTCA. At the time of coronary angiography if partially occlusive thrombus is identified, intravenous heparin and aspirin should be given to prevent more thrombus formation and total occlusion.

Angina Pectoris↗
PubMed1988

Effect of intravenous isosorbide dinitrate versus nitroglycerin on elevated pulmonary arterial wedge pressure during acute myocardial infarction.

To compare the acute and sustained effect of intravenous isosorbide dinitrate to intravenous nitroglycerin in patients with acute myocardial infarction and elevated pulmonary artery wedge pressure, 111 patients were randomized and studied within 96 hours of admission to the coronary care unit. All patients had a pulmonary artery wedge pressure greater than or equal to 10 mm Hg and received either isosorbide dinitrate (74 patients) or nitroglycerin (37 patients) for 24 to 48 hours. Blood pressure, heart rate, pulmonary artery wedge pressure, cardiac output, medication dose in micrograms per minute and retitration episodes were compared at baseline and at 6, 12, 18 and 24 hours. Both drugs significantly (p less than 0.05) lowered pulmonary artery wedge pressure and blood pressure and increased cardiac output. Isosorbide dinitrate required fewer retitration episodes and less increases in dosage than nitroglycerin at 24 hours. In the patient with acute myocardial infarction complicated by high pulmonary artery wedge pressure who requires intravenous nitrates for 24 hours, isosorbide dinitrate may offer the benefit of a more stable hemodynamic effect.

Aged↗
PubMed1988

Coronary artery spasm and its relationship to exercise in patients without severe coronary obstructive disease.

Coronary artery spasm is reported to occur with exercise. In patients without severe coronary atherosclerosis, the evidence for exercise-induced coronary artery spasm is limited. Three patients with positive exercise tests but no severe coronary atherosclerosis are presented. Coronary artery spasm was provoked and verified by angiography in all three, but coronary angiography during exercise failed to demonstrate spasm. The literature is reviewed and the value of a routine protocol for evaluation is discussed.

Adult↗
PubMed1988

Silent myocardial ischemia: prognostic significance and therapeutic implications.

Evidence is now accumulating which strongly suggests that prognosis of patients with painless myocardial ischemia determined either by ambulatory ECG monitoring or exercise testing may be no different than the prognosis of patients who have overt clinical manifestations of myocardial ischemia associated with transient ischemic ECG changes. In my view the goal of therapy for patients with clinical manifestations of coronary artery disease should be the elimination of myocardial ischemia. Medical therapy, coronary angioplasty, or coronary artery surgery should be rendered and then followed by objective documentation of therapeutic efficacy.

Coronary Disease↗
PubMed1987

Use of nitrates in unstable angina pectoris.

The rationale for using intravenous nitrates in patients hospitalized with severe angina pectoris is that physiologic action is almost immediate. Many studies and clinical experience indicate that the use of this preparation results in a marked diminution of recurrent angina episodes in most patients. If adverse reactions such as severe hypotension or bradycardia occur, decreasing the dose or stopping it entirely corrects the problem. Intravenous nitroglycerin can be used in combination with other known antianginal agents, such as beta blockers and calcium antagonists. In clinical practice most patients are treated with nitrates and beta blockers or calcium antagonists because the combination of drugs may reduce ischemia and symptoms more than each drug used alone over a long period.

Administration, Oral↗
PubMed1987

Assessment of left ventricular wall thickness in healed myocardial infarction by magnetic resonance imaging.

The ability of magnetic resonance imaging (MRI) to detect and localize healed myocardial infarction (MI) was assessed. Seventeen consecutive patients with healed MI assessed by biplane contrast ventriculography underwent MRI using oblique imaging planes. Seven normal subjects underwent MRI as controls. In each patient, ventriculography identified regional wall motion abnormalities. MRI, performed with a 0.15-Tesla resistive magnet and oblique imaging planes relating to the left ventricle, detected zones of regional wall thinning conforming to the wall motion abnormalities localized by ventriculography in 16 patients. In these patients, adjacent areas of intact myocardium were identified in areas shown by ventriculography to be normal. The left ventricular wall thickness at the site of MI was significantly less than adjacent noninfarcted myocardium (p less than 0.001) and normal hearts (p less than 10(-6)). The ratio of the thickness of the infarct to adjacent normal wall averaged 0.40 (range 0.22 to 0.62). MRI could differentiate healed MI from adjacent noninfarcted myocardium and normal hearts.

Adult↗
PubMed1987

Reduction in myocardial neutrophil accumulation and infarct size following administration of thromboxane inhibitor U-63,557A.

We examined the effects of a new selective thromboxane A2 (TXA2) synthetase inhibitor, U-63,557A, on myocardial infarct size 48 hours following left coronary ligation in rats. With a single 8 mg/kg dose of U-63,557A (furegrelate) administered prior to coronary ligation, platelet aggregation and serum TXA2 formation declined significantly (p less than 0.02) for up to 48 hours. Myocardial infarct size, as measured by planimetry of serial left ventricular sections, was decreased from 44 +/- 3% (saline-treated control rats) to 34 +/- 4% (p less than 0.05). Left ventricular creatine kinase (CK) following coronary ligation was also preserved in U-63,557A vs saline-treated control animals (p less than 0.05). These beneficial effects of U-63,557A were not accompanied by reduction in the indices of myocardial oxygen demand (heart rate and arterial pressure). Furthermore, neutrophil accumulation in the infarcted myocardium was significantly decreased by U-63,557A (26 +/- 6 vs 96 +/- 3/high-power field [p less than 0.01]). These data suggest that administration of a single dose of selective TXA2 synthetase inhibitor prior to coronary ligation modulates platelet function for up to 48 hours and reduces the extent of myocardial injury, which may, in part, relate to decrease in neutrophil accumulation.

Animals↗