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Biomedical subjects

C R Conti

Publications and source records attributed to C R Conti.

At least 325 records · Page 18Linked to original sources
PubMed1981

Regional coronary angiographic observations during cold stimulation in patient with exertional chest pain: comparison of diameter responses in normal and fixed stenotic vessels.

In 12 patients with exertional chest pain, coronary angiography was performed and quantitative measurements coronary artery (CA) diameters were made before and during cold stimulation (four normal CA patients and eight fixed CA stenosis patients). The left main CA; proximal, middle and distal anterior descending and circumflex segments; and small intramyocardial CAs (0.4 to 1.0 mm) usually showed only minimal and similar degree of vasoconstriction (average diameter reduction 6%) during cold stimulation in both normals and CA disease (CAD) patients. Magnitude of vasoconstriction differed among some CA segments measured; the left main CA segment (0 +/- 2%, mean +/- SD) usually did not change while distal segments (-10 +/- 10%) usually demonstrated greatest percentage vasoconstriction. Coronary stenoses and CAs filled by collaterals did not demonstrate increased magnitude of vasoconstriction compared to other CAs. Results of other CA segments were also similar comparing patients with and without CAD. The minimal degree of vasoconstriction observed in these CA segments does not appear to account for the large increase in coronary resistance reported during cold stimulation in CAD patients.

Cardiac Catheterization↗
PubMed1981

Effects of prostacyclin on systemic and coronary hemodynamics in the dog.

The hemodynamic effects of intravenous and intracoronary prostacyclin (PGI2) were evaluated in anesthetized, open-chest instrumented dogs. Coronary artery and aortic blood flows, aortic and left ventricular (LV) diastolic pressure, and heart rate were measured continuously. With intravenous PGI2 both left anterior descending (LAD) and circumflex (LCX) coronary artery blood flows remained unchanged; both arterial and LV diastolic pressures declined; coronary resistance declined progressively with increasing PGI2; peak reactive hyperemic flow following 10-second coronary artery occlusion declined progressively with increased PGI2; heart rate responses were variable at low doses but increased at high dose; and aortic blood flow increased consistently. With intracoronary PGI2 both LAD and LCX coronary blood flows increased promptly in dose-related manner. In dogs with critical coronary artery narrowing (loss of reactive hyperemia) created by an external plastic occluder, intravenous prostacyclin (0.5 microgram/kg/min) did not alter flow in narrowed coronary artery, but increased flow in the non-narrowed coronary artery (p less than 0.02) as both systemic arterial and LV diastolic pressure declined. These results show that PGI2 has potent direct coronary and systemic vasodilator actions.

Animals↗
PubMed1981

Effect of diltiazem in patients with variant angina: a randomized double-blind trial.

Effects of diltiazem of frequency of angina and nitroglycerin (NTG) consumption were studied in 12 patients with variant angina (rest pain with ST elevation). Either diltiazem in two dosage schedules (120 mg/day and 240 mg/day), or placebo was administered in a randomized double-blind program over 10 weeks. Significant decreases in angina frequency and TNG consumption were observed when diltiazem treatment periods were compared to placebo periods. Furthermore, when placebo periods following diltiazem were compared to placebo periods following placebo, significant "carry-over" effect with respect to reduced angina frequency was observed. No patient had an increase in angina frequency or TNG consumption on diltiazem compared to placebo. No "rebound effects" or changes in blood pressure or heart rate were observed. One patient complained of dry mouth on diltiazem. These findings, although in a limited number of patients, suggest that diltiazem is effective in decreasing angina frequency and TNG consumption in patients with variant angina. These encouraging results warrant evaluation of diltiazem in a larger patient population over a longer time period.

Adult↗
PubMed1981

Platelet function studies in coronary artery disease. X. Effect of dipyridamole.

To evaluate the effects of dipyridamole on blood platelet function in patients with coronary artery disease, platelet counts and aggregation were examined in aortic and coronary venous blood. Before administration of dipyridamole, platelet counts and aggregation in response to adenosine diphosphate were less (p less than 0.02) in coronary venous than in aortic blood. Dipyridamole administration (100 mg) resulted in an increase in platelet counts and platelet aggregation in coronary venous blood so that the differences in aortic and coronary venous blood values were eliminated. These phenomena were probably related to inhibitory actions of dipyridamole on platelet adhesion to atherosclerotic vessels. To further study the mechanism of action, the direct effects of dipyridamole on in vitro platelet aggregation were evaluated. Although dipyridamole, in the concentrations used, had no effect on in vitro platelet aggregation, it greatly potentiated the aggregation inhibitory actions of exogenous prostacyclin. In vivo potentiation of endogenous prostacyclin and inhibitory actions on platelet adhesion are the most likely mechanisms of the potentially beneficial actions of dipyridamole.

Adenosine Diphosphate↗
PubMed1981

Short-term efficacy of oral verapamil in rest angina. A double-blind placebo controlled trial in CCU patients.

To determine the efficacy and safety of oral verapamil in patients with rest angina admitted to the Coronary Care Unit (CCU), a double-blind placebo-controlled trial was undertaken. Of the 65 patients with rest angina screened for the study, 15 met the inclusion criteria (at least two episodes of chest pain associated with ST-T segment changes per 24 hours) during single-blind placebo phase (Day 1). Patients were then randomized to receive either placebo or verapamil (80 mg every 6 hours) on Day 2. Protocol was designed such that those who did not respond to the placebo (nonresponders) received verapamil, 80 mg every 6 hours, whereas verapamil nonresponders received increased doses (120 mg every 6 hours) on Day 3. Those who did respond (responders) continued to receive their medication. Similar action was taken on Day 4, depending on chest pain frequency and clinical evaluation. The study drug was unblinded on Day 4. At the end of the four-day period, 13 patients were receiving verapamil (nine patients, 80 mg every 6 hours, and four patients, 120 mg every 6 hours) and all but one were responders. One patient received placebo all through the period of the study and was also considered to be a responder. In the remaining one patient evidence of myocardial necrosis developed after he received a single dose of verapamil (80 mg on Day 2). Except for the prolongation of PR interval in two patients while taking verapamil, no side effects from verapamil therapy were observed. These data demonstrate the efficacy of oral verapamil in reducing episodes of myocardial ischemia in the majority of all patients with rest angina.

Administration, Oral↗
PubMed1981

Magnitude of dilatation of large and small coronary arteries of nitroglycerin.

Vasodilatory responses of segments of large epicardial left coronary artery (CA), small intramyocardial CAs (0.3-1.0 mm), coronary stenoses and CAs filled by collaterals were determined in 34 patients. Measurements were made before and after nitroglycerin (0.4 mg, sublingual) by means of quantitative magnification coronary angiography using photospot film and a calibrated 6-power viewing device. The left main CA, proximal, middle and distal anterior descending and circumflex segments, and small CAs showed dilatation that varied in magnitude. When magnitude of dilatation was compared with control diameter of the vessel and its location, control diameter proved to be the significant independent variable. CAs with the smallest control diameter showed the greatest magnitude of vasodilatation. CA branches filled by collaterals had vasodilatation similar in magnitude to that of CAs of comparable control diameter. Although coronary stenoses dilated, the magnitude of dilatation was less than that observed in nonstenosed arterial segments of similar control diameter. When areas of stenosis were excluded, however, results were similar regardless of whether the patient had CA disease. These data indicate that a principal determinant of the CA vasodilatory response to nitroglycerin is the size of the artery before nitroglycerin.

Adult↗
PubMed1981

Acute effect of intravenous dipyridamole on regional coronary hemodynamics and metabolism.

The acute coronary hemodynamic and metabolic effects of intravenous dipyridamole were studied in 13 patients. Total left ventricular (LV), anterior (supplied by the left anterior descending coronary artery) and inferior (supplied by circumflex and right coronary arteries) regional flows and metabolic responses were assessed from the coronary sinus and great cardiac vein. Perfusion to LV regions was classified as potentially "normal" or "abnormal," based on coronary angiographic findings. Before dipyridamole, coronary flow, LV oxygen delivery and lactate extraction in both the normal and abnormal regions were similar. Within 1 minute after injection of 20 mg of dipyridamole by i.v. bolus, total coronary flow increased 51% (p less than 0.05). Fifteen minutes after injection the flow increase persisted. Flow decreased to approximately control level by 20 minutes. The major component of this increased total coronary flow resulted from increased flow in normal regions (75% at 1 minute, p less than 0.05). Mean regional LV oxygen delivery and lactate extraction were not changed significantly in either normal or abnormal regions. However, lactate production occurred more often after dipyridamole in abnormal regions. These results suggest that during dipyridamole-induced hyperemia, regional coronary flow and metabolic responses depend upon the status of the arteries supplying the LV region. Regional differences in flow and metabolism occur independent of major changes in heart rate and aortic and LV pressures.

Adult↗
PubMed1981

Quantitation of aortic insufficiency using a catheter-tip velocity transducer.

Bidirectional instantaneous aortic root blood flow was measured in 18 patients with aortic insufficiency (AI) using a catheter-tip velocity transducer. The magnitude of AI was quantitated by determining total forward systolic flow from the area of the flow velocity curve above the zero baseline and regurgitant diastolic flow from the curve area below the baseline. Effective forward flow (stroke volume) was calculated as the difference between total forward systolic flow and regurgitant diastolic flow. Regurgitant fraction was determined as the ratio of regurgitant flow to total forward flow. These data were compared with conventional angiographic estimates (1+ to 4+) of the degree of insufficiency. Velocity transducer determination of regurgitant fraction was 26% in the patient with 1+ AI, 37% (31-48%) in 2+ AI, 49% (35-61%) in 3+ AI and 72% in 4+ AI (regurgitant fraction vs angiographic grade, r = 0.84). Regurgitant flow per diastole was 9 ml in the patient with 1+ AI, 39 ml (20-49 ml) in 2+ AI, 57 ml (31-102 ml) in 3+ AI and 183 ml (143 and 223 ml) in 4+ AI (regurgitant diastolic flow vs angiographic grade, r = 0.73). Good correlation (r = 0.90) was found between values of regurgitant flow obtained from the left ventriculogram and those obtained using the velocity transducer. Although the overall association was good, wide, variability in regurgitant fraction and regurgitant flow was found in the 15 patients with 2+ to 3+ AI. These results suggest that the electromagnetic velocity catheter offers a simple technique for quantitating AI.

Adolescent↗
PubMed1981

Pathogenesis and pathophysiology of ischemic heart disease.

Animal experiments illustrating the effects of coronary artery disease are described. These experiments show marked blunting of reactive hyperremia with 80% of narrowing, and markedly decreased resting blood flow with 90% narrowing of the coronary artery. With 60% stenosis, blunting of hyperemic response occurs with a 5 mm long stenosis and decreased resting blood flow with a 10 mm long stenosis. Further reduction of resting blood flow is demonstrated with serial narrowing. In 6 patients with variant angina, resting myocardial blood flow decreased during episodes of spontaneous angina. Similar results were found in 13 patients with variant angina after ergonovine administration.

Animals↗
PubMed1980

Platelet function studies in coronary heart disease. IX. Increased platelet prostaglandin generation and abnormal platelet sensitivity to prostacyclin and endoperoxide analog in angina pectoris.

Platelet prostaglandin generation (malondialdehyde production) and platelet sensitivity to prostacyclin (a vasodilator and platelet aggregation inhibitor) and to epoxymethanodienoic acid (EMA) (a vasoconstrictor and platelet aggregation stimulant endoperoxide analog) were studied in patients with angina pectoris and in control subjects. Platelet malondialdehyde production was higher in patients than in control subjects (mean +/- standard error of the mean 2.50 +/- 0.30 versus 1.70 +/- 0.13 nmol/10(9) platelets, p < 0.02). Platelets from patients were significantly less sensitive to prostacyclin's antiaggregatory effects than were those from control subjects (amount of prostacyclin required for 50 percent platelet aggregation inhibition 1.90 +/- 0.35 versus 0.68 +/- 0.05 ng, p < 0.02). Furthermore, less EMA was required to induce 50 percent platelet aggregation in patients with angina pectoris than in the normal subjects (133 +/- 8 versus 194 +/- 16 ng, p < 0.001). These observations suggest that increased platelet prostaglandin generation and abnormal platelet sensitivity to prostacyclin and endoperoxide analog in certain patients with coronary artery disease are important potential mechanisms in the pathogenesis of myocardial ischemia.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗