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Biomedical subjects

C R Conti

Publications and source records attributed to C R Conti.

At least 235 records · Page 13Linked to original sources
PubMed1987

Coronary artery spasm.

Coronary artery spasm is a transient reduction in lumen diameter of an epicardial coronary artery of sufficient degree to produce objective evidence of myocardial ischemia in the absence of any significant increase in heart rate or blood pressure. In this article are summarized pathophysiological observations, the coronary angiographic anatomy of patients with coronary spasm, etiologic considerations, methods to provoke coronary artery artery spasm and their clinical usefulness, the role of coronary artery spasm in patients with clinical angina pectoris and myocardial infarction, and finally, the role of coronary artery spasm in patients undergoing coronary artery surgery.

Coronary Vasospasm↗
PubMed1987

Heart transplantation candidates: psychological evaluation.

Most medical centers that perform heart transplantation have established medical review boards that consider medical, psychosocial, and financial factors in choosing appropriate candidates. The psychological evaluation described here can furnish clinically useful baseline data regarding the patient's emotional and cognitive functioning, and identify other individual and family variables that may affect patient compliance and the outcome of transplantation.

Attitude to Health↗
PubMed1987

Acute myocardial ischemia: role of atherosclerosis, thrombosis, platelet activation, coronary vasospasm, and altered arachidonic acid metabolism.

Potential causes for the development of acute myocardial ischemia include extracardiac factors, rapid progression of atherosclerosis, dynamic coronary artery thrombosis, platelet activation in diseased vessels, abnormal constriction of a coronary artery, and abnormal arachidonic acid metabolism. It is entirely possible that all or many of these potential causes may be occurring in the individual patient.

Acute Disease↗
PubMed1986

Left ventricular dyskinesia reversed by intravenous nitroglycerin: a manifestation of silent myocardial ischemia.

Patients with coronary artery disease (CAD) frequently have left ventricular (LV) wall motion abnormalities in the absence of symptoms. Thirty-one patients with such LV wall motion abnormalities in the absence of symptoms participated in a study of the response of these abnormalities to ascending doses of intravenous nitroglycerin (NTG). In a subgroup of 20 patients the relation between the location of LV wall motion abnormalities and the presence or absence of significant CAD (greater than or equal to 50% diameter reduction), in the vessel supplying the LV region, was assessed. Wall motion improved after intravenous NTG; the ejection fraction increased by 3.7% (mean p less than 0.05) and by 9.4% in the 19 patients who responded. There was no significant increase in heart rate; both LV systolic and end-diastolic pressures decreased minimally (12.5 and 3.5 mm Hg, respectively, p less than 0.05). The ejection fraction response was observed with NTG doses less than or equal to 200 micrograms and no dose-response relation was apparent. In the subgroup subjected to regional wall motion analysis, the presence of dyskinesia was significantly (p = 0.007) associated with the presence of important CAD in a vessel supplying that region. Further, the fact that wall motion improvement after NTG was significantly (p = 0.002) associated supports the concept that silent ischemia results in LV regional wall motion abnormalities, which can be reversed with low dose intravenous NTG.

Adult↗
PubMed1986

Percutaneous transluminal coronary angioplasty in evolving acute myocardial infarction.

In 29 patients with evolving acute myocardial infarction, acute reperfusion of the infarct-related coronary artery was attempted using percutaneous transluminal coronary angioplasty (PTCA). Before PTCA, angiography showed 23 totally occluded and 6 severely stenotic infarct-related coronary arteries. PTCA was initially successful in 25 of 29 patients (86%). Reocclusion occurred in 4 patients within 12 hours after successful PTCA and was associated with new electrocardiographic changes or recurrence of symptoms. In 17 patients the infarct-related coronary artery remained patent at early follow-up; late stenosis occurred in 4 patients. Recurrence of stenosis was accompanied by development of angina. No clinical or angiographic features distinguished those with ultimate vessel patency, occlusion or recurrence of stenosis. On follow-up, ventricular function appeared better preserved or improved in those with a patent infarct-related coronary artery than in those with an occluded infarct-related coronary artery. Further studies are warranted to compare PTCA and streptokinase as primary reperfusion modalities in evolving acute myocardial infarction.

Adult↗
PubMed1986

Transluminal laser irradiation of coronary arteries in live dogs: an angiographic and morphologic study of acute effects.

In vivo coronary transluminal laser irradiation, using energies known to vaporize atherosclerotic plaques and thrombi, was performed in normal coronary arteries of 5 anesthetized mongrel dogs. A 200-mu core silica optical fiber with a radiopaque tip was advanced through a catheter to either the left anterior descending or circumflex coronary arteries. Coronary artery perforation occurred during manipulation of the fiber in 1 dog. In 4 dogs, argon laser radiation was delivered at 1-second intervals. A total of 45 different sites were irradiated in 8 coronary arteries. In 5 of these arteries 1 W was used and in the 3 other arteries 2 W were used. Coronary angiography showed perforation of 5 of these 8 arteries. Two arteries were perforated using 1 W and 3 using 2 W. Within 30 minutes, 3 dogs with perforation died of cardiac tamponade. In all 4 dogs postmortem examination showed perivascular blood extravasation around all 8 lased coronary arteries. Transluminal lasing of normal dog coronary arteries using delivery systems and energies similar to those known to vaporize atherosclerotic plaques and thrombi resulted in arterial perforation, frequently followed by cardiac tamponade.

Angiography↗
PubMed1986

Laser angioplasty with angioscopic guidance in humans.

An experimental study was conducted in 11 patients to evaluate the immediate effects of laser recanalization during peripheral arterial bypass surgery. Angioscopy allowed precise localization and identification of the occlusion. A 1 or 2 mm optical fiber probe was used. Laser energy was regulated using the least amount of energy necessary for recanalization. New vascular channels were made in 10 of the 11 patients. After recanalization the arterial segment was excised for histologic evaluation. Smaller channel diameters were made with the 1 mm probe (1.5 +/- 0.6 mm) than with the 2 mm probe (3 +/- 0.3 mm) (p less than 0.05). Flow through channels (mean pressure 80 mm Hg) made with the 2 mm probe was greater than that through channels made with the 1 mm probe (150 +/- 102 versus 19.7 +/- 10 cc/min) (p less than 0.05). The amount of debris formed was small with both probes. Vascular perforations were less frequent with the 2 mm probe (two of nine arteries) compared with the 1 mm probe (four of four arteries). Successful recanalization with flow rates expected to maintain vascular patency was achieved only with the 2 mm probe. Histologic studies at nonperforated sites demonstrated that the elastica of the artery appeared to be preserved whereas the overlying plaque and underlying media were thermally disrupted. This suggests that the elastic tissue acts as an optical window allowing the argon beam to go through it without causing morphologic damage. Except for fresh thrombus, atheromas including calcific plaque and old organized thrombus were readily vaporized. These results are encouraging for the use of the laser for vascular recanalization in humans.

Aged↗
PubMed1986

Early post infarction angina: therapeutic strategies.

The approach to the patient with post-infarction recurrent angina pectoris should be systematic and logical. In order to treat the patient appropriately, one must understand the pathogenetic mechanisms responsible for recurrent angina. Coronary angiography must be performed principally to determine the extent of coronary artery disease, and presence or absence of thrombosis, abnormal constriction of a conductive coronary artery, or mechanical dysfunction of the heart. Extracardiac (aggravating) factors and mechanical abnormalities that increase myocardial oxygen demand must be corrected appropriately. If coronary artery spasm is present, vasodilator therapy is appropriate. If recurrent thrombosis is found or a patent vessel with a residual high-grade (90%) stenosis is present, performance of PTCA in the affected artery seems logical in order to prevent recurrence of myocardial infarction.

Angina Pectoris↗
PubMed1986

Effect of propranolol on myocardial ischemia occurring during acute coronary occlusion.

In 16 patients undergoing angioplasty of the left anterior descending coronary artery, the clinical, electrocardiographic, and hemodynamic effects of short-term intravenous nonselective beta-adrenergic blockade with propranolol (0.1 mg/kg) were assessed during temporary occlusion of the artery. Myocardial ischemia during coronary occlusion was prevented, delayed in onset, or diminished in magnitude by propranolol in 10 of the 16 patients. Propranolol decreased values for indexes of myocardial oxygen demand, such as heart rate and blood pressure and their product, in all patients. Surprisingly, in patients who derived clinical benefit, propranolol did not change indexes of myocardial oxygen supply to the left ventricular region perfused by the occluded artery. For example, great cardiac vein flow (40 +/- 15 to 41 +/- 17 ml/min, p = NS) and coronary collateral resistance (2.1 +/- 1.0 to 2.1 +/- 1.1 mm Hg/ml/min, p = NS) were unchanged. In contrast, a worsening of supply occurred in patients who were not benefited: great cardiac vein flow (50 +/- 10 to 39 +/- 6 ml/min, p less than .05) decreased and coronary collateral resistance (1.6 +/- 0.5 to 2.0 +/- 0.6 mm Hg/ml/min, p less than .05) increased. Information obtained from this study demonstrates the value of this new experimental preparation in helping assess potential clinical effectiveness of drug interventions during the initial phase of acute coronary occlusion and providing insight into the mechanisms of drug effect.

Adult↗
PubMed1986

Ventricular/vascular interaction in patients with mild systemic hypertension and normal peripheral resistance.

Total left ventricular external power and aortic input impedance spectra were calculated from recordings of pulsatile pressure and flow in the ascending aorta of 22 human subjects undergoing cardiac catheterization. Eleven subjects had increased aortic pressure (systolic 153 +/- 3.8[SEM] mm Hg, p less than .001; diastolic 91 +/- 2.4 mm Hg, p less than .03; mean 118 +/- 2.4 mm Hg, p less than .001) and constituted the group with mild hypertension (average age 50 +/- 1.9 years). The other 11 (age-matched) subjects had normal arterial pressures and constituted the control group. Cardiac output in the hypertensive group was abnormally high (6.9 +/- 0.3 liters/min, p less than .04) compared with that in control subjects (6.1 +/- 0.2 liters/min), so that peripheral resistance was similar. Characteristic aortic impedance (index of aortic elastance) was increased in the hypertensive group (142 +/- 19 vs 72 +/- 4.5 dyne-sec-cm-5, p less than .002), as was the fluctuation of impedance moduli and phase. These elevated pulsatile components of arterial load were associated with a significant (p less than .002) increase in pulsatile left ventricular external power (89%), and the increased cardiac output was associated with a significant (p less than .001) increase in steady flow power (31%). The ratio of pulsatile to total power was also increased (38%) in the hypertensive group (p less than .001). Increased characteristic aortic impedance in the hypertensive group suggests that the human aorta is stiffer, and fluctuations in the impedance spectra suggest increased or less dispersed wave reflections.(ABSTRACT TRUNCATED AT 250 WORDS)

Aorta↗
PubMed1986

Unstable angina before and after infarction: thoughts on pathogenesis and therapeutic strategies.

The pathophysiology of unstable angina both before and after infarction is incompletely understood, because the patient population with the diagnosis of unstable angina is not uniform and the definition of this condition is not precise. The question must be asked, "Why does a patient suddenly become unstable?" Several conditions can be responsible alone or in combination with each other. These conditions include extracardiac (aggravating) factors, rapid progression of coronary atherosclerosis, rapid decrease in coronary lumen size as a result of hemorrhage into an atherosclerotic plaque, transient platelet aggregation in severely diseased vessels, transient coronary artery thrombosis, and abnormal coronary artery vasoconstriction (spasm) in normal or diseased vessels. Fig. 1 summarizes a hypothetical scheme relating the above conditions to the degree of coronary artery stenosis. In patients with unstable angina before infarction, most investigators believe that severe coronary atherosclerosis and its consequences are the major pathogenic mechanisms when ischemic heart disease is present. If spasm is the mechanism, then the use of vasodilators is warranted. However, if thrombosis is clearly defined, then thrombolytic therapy in the early stages seems reasonable. If severe coronary artery disease is found (with or without thrombosis), therapy with anticoagulants such as intravenous heparin during the acute phase of the illness can be argued strongly. A similar argument could be made for the use of antiplatelet agents during the convalescent phase. If extracardiac (aggravating) factors are present, they must be corrected appropriately.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1986

Left ventricular function abnormalities as a manifestation of silent myocardial ischemia.

A large body of evidence exists indicating that left ventricular dysfunction is a common occurrence in patients with severe coronary artery disease and represents silent or asymptomatic myocardial ischemia. Such dysfunction probably occurs early in the time course of every ischemic episode in patients with coronary artery disease whether symptoms are eventually manifested or not. The pathophysiology of silent versus symptomatic left ventricular dysfunction due to ischemia appears to be identical. Silent ischemia-related left ventricular dysfunction can be documented during spontaneous or stress-induced perturbations in the myocardial oxygen supply/demand ratio. It also may be detected by nitroglycerin-induced improvement in ventricular function or by salutary changes in wall motion following revascularization. Silent left ventricular dysfunction is a very early occurrence during ischemia and precedes electrocardiographic abnormalities. In this light, its existence should always be kept in mind when dealing with patients with ischemic heart disease. It can be hypothesized that because silent ischemia appears to be identical to ischemia with symptoms in a pathophysiologic sense, prognosis and treatment in both cases should be the same.

Coronary Disease↗
PubMed1986

Evaluation and treatment of the asymptomatic patient with a positive exercise tolerance test.

A positive exercise study in an asymptomatic patient presents a clinical dilemma. Many of these asymptomatic positive studies are false-positive, but a subset of these patients have silent coronary artery disease. Other noninvasive tests can be used in conjunction with exercise testing to help identify this subset of patients, but coronary angiography is often ultimately necessary to ensure an accurate diagnosis. An algorithm for the evaluation and treatment of the patient with an asymptomatic positive exercise study is proposed.

Angiography↗