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Biomedical subjects

C R Conti

Publications and source records attributed to C R Conti.

At least 271 records · Page 15Linked to original sources

Laser recanalization of occluded atherosclerotic arteries in vivo and in vitro.

Controlled laser irradiation was used to recanalize atherosclerotic stenoses in vivo and in vitro. In 15 rabbits with atherosclerotic arteries a catheter was positioned in the distal aorta for angiographic examination and as a guide for a small silica optical fiber. Both Nd-YAG and argon lasers were used for recanalization with varying power and duration. As determined by angiographic studies the severity of iliofemoral stenoses in eight 15 arteries decreased from 78 +/- 18% to 32 +/- 11% (mean +/- SD). In one additional artery the stenosis improved from 45% to 25%, but this was associated with perforation. The other six arteries were perforated (two after fiber manipulation, four after laser discharge) without obvious improvement in severity of stenosis. No angiographic loss of distal circulation was noted. To better define tissue- laser interactions in the live-rabbits, lasing of 15 totally occluded atherosclerotic rabbit arterial segments in vitro was done while the optical fiber was advanced or fixed. When the fiber was fixed, serial sections showed that the new lumen was flame shaped. The width and depth of the lumen increased with increasing laser energy. When the fiber was advanced, histologic examination showed a smooth cylindrical vascular channel with limited lateral tissue damage. This study demonstrated that lasers can recanalize atherosclerotic stenoses in a live animal preparation; however, arterial perforation remains a problem.

Animals↗

Effect of nitroglycerin on coronary collateral flow and pressure during acute coronary occlusion.

Coronary collateral function was evaluated in 21 conscious, unsedated patients by measuring aortic and distal coronary pressures and great cardiac vein flow during transient (1 minute) balloon occlusion of the anterior descending artery in the course of coronary angioplasty. Measurements were made before and during administration of intravenous nitroglycerin (NTG). Clinical, electrocardiographic and hemodynamic events of transient myocardial ischemia occurred in 10 patients before and 6 patients during NTG administration (p = 0.11). The NTG infusion consistently decreased pressure determinants of myocardial oxygen demand without increasing heart rate. NTG also decreased a calculated coronary collateral resistance index in 13 patients. Responsiveness to NTG did not appear to depend on the presence or absence of collateral vessels detected by angiography or on any other angiographic variable assessed. Measurement of coronary collateral function during coronary angioplasty is a new technique with the potential to assess the ability of interventions to prevent transient myocardial ischemia and improve myocardial perfusion during acute coronary occlusion in humans.

Adult↗

Effects of acute coronary occlusion on hemodynamics in an adjacent coronary artery in dogs.

The effects of acute occlusion of 1 coronary artery on flow responses in another were studied in 24 open-chest dogs. Left circumflex (LC) flow was measured with and without LC stenoses before and during reactive hyperemia. In 19 dogs the left anterior descending artery (LAD) was occluded and measurements were repeated after 1 hour (group 1). Four dogs had measurements before and after 1 hour without LAD occlusion (group 2). In group 2 no systemic, left ventricular (LV) or coronary hemodynamic changes were observed after 1 hour. In group 1, an hour after LAD occlusion, heart rate and aortic pressure had not changed but stroke volume decreased slightly (-8 +/- 7%, mean +/- SD, p = not significant) and LV end-diastolic pressure had increased (2 +/- 3 mm Hg, p less than 0.05). Basal LC flow was not changed by less than 90% LC stenosis. Ninety percent LC stenosis decreased LC flow both before and after LAD occlusion. During reactive hyperemia without LC stenosis, LC flow decreased after LAD occlusion in 15 of 19 dogs (from 154 +/- 80 to 141 +/- 75 ml/min, p less than 0.05). With 60 and 80% LC stenoses, LC flow during reactive hyperemia decreased before LAD occlusion (110 +/- 62 and 74 +/- 40 ml/min, respectively), but decreased further (both p less than 0.05) after LAD occlusion (98 +/- 54 and 63 +/- 43 ml/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Left ventricular changes resulting from chronic aortic regurgitation in dogs.

Chronic aortic regurgitation (AR) was induced by aortic valve perforation using catheterization techniques in 7 closed-chest puppies. Approximately 2 years after the creation of AR in these puppies, their growth was similar to that in littermate controls. A gradually progressive degree of left ventricular (LV) dilation and hypertrophy occurred as LV end-diastolic volume (average 116%) and mass (average 114%) increased in animals with AR compared with that in the littermate controls. The technique described to induce AR did not interfere with the normal growth and development of the animals, and permitted study of the functional characteristics of the resulting LV dilation and hypertrophy without added effects of thoracotomy and pericardiotomy.

Animals↗

Evaluation of a three-dimensional reconstruction to compute left ventricular volume and mass.

This study tests the accuracy of a model to calculate left ventricular volume (LVV) and muscle volume (MV) when optimal data were used. These volumes were calculated using endocardial and epicardial borders traced from photos of cross sections of 20 animal (dog, goat and pig) hearts. A pyramid summation algorithm was used to perform a 3-dimensional (3-D) reconstruction based on 5 short-axis views, thus providing computer volume estimates. These were compared with the true (T) ventricular volumes determined by water filling of the cavity and the true MV based on weight. Because each heart was sliced in 5 planes, the appropriateness of the algorithm for MV could be tested for 6 regions. The pyramid summation algorithm consistently underestimated MV at the base and apex, but was accurate from the midmitral valve to the inferior papillary muscle region. Consequently, the total MV was computed as the midventricular MV, plus base and apex volumes computed from regression equations. Results showed that 3-D reconstruction resulted in a regression of LVVT = 1.02LVV3D + 10.30 ml with r = 0.987 for the chamber of MVT = 1.05 MV3D - 9.78 ml, with r = 0.967. It is concluded that the pyramid summation algorithm can accurately estimate volumes from spatially registered short-axis data with 95% prediction limits about the mean of the data of +/- 10 ml for left ventricular chamber volume and +/- 17.6 ml for MV.

Animals↗

A new model for investigation of transluminal recanalization: human atherosclerotic coronary artery xenografts.

A model for testing transluminal recanalization techniques was developed. Human atherosclerotic arteries were transplanted in dogs and evaluated by angiographic and histologic study within a 12-week period. An inflammatory response was most intense within the first 2 weeks. By 12 weeks, no inflammation was noted. The model has several advantages: (1) The pathologic characteristics are those of a human coronary artery. (2) Thrombus formation is frequent, with progression to a well organized dense fibrocellular vascular occlusion within 4 to 12 weeks. (3) The arterial occlusion resembles human vascular disease. (4) The vascular occlusions are readily accessible with standard catheterization technique. (5) The model is easy to produce within a short period. This model has been used to evaluate laser recanalization of vascular obstructions.

Angiography↗

In vitro analysis of boundary identification techniques used in quantification of two-dimensional echocardiograms.

Echocardiographic cross-sectional areas of 10 formalin-fixed animal left ventricles were determined by 5 independent observers using black-white (B-W) and mid-spot (M-S) endocardial boundary identification techniques. The echocardiographic cross-sectional areas were compared with the true anatomic cross-sectional areas of the same 10 hearts to determine the accuracy, variability and reliability of each technique. The results of these comparisons revealed that the M-S technique was more accurate than the B-W technique (3.3 +/- 7.2 vs 34.9 +/- 8.6% error). However, the B-W technique was more reliable in that it had a smaller interobserver and estimated intraobserver variability. The M-S technique had a 6% greater intraobserver variability.

Animals↗

Effects of bepridil on exercise tolerance in chronic stable angina: a double-blind, randomized, placebo-controlled, crossover trial.

Bepridil, a calcium antagonist with a half-life of approximately 42 hours, was compared with placebo in a double-blind, randomized, crossover trial. Thirteen men (average age 62 years) with exercise-related angina pectoris and a positive exercise test (modified Bruce protocol) were studied. In the group as a whole, bepridil (400 mg once a day) caused an increased total exercise time (2.6 +/- 1.8 minutes, mean +/- standard deviation), time to onset of angina (3.3 +/- 1.6 minutes), time to 1 mm of ST-segment depression (2.2 +/- 2.3 minutes), time to 2 mm of ST-segment depression (2.4 +/- 1.4 minutes) and total work load achieved (1.8 +/- 1.4 kpm) compared with the preceding placebo phase (all p less than 0.05). Frequency of angina and nitroglycerin consumption were low and did not change significantly during bepridil therapy. Comparison of the 3 placebo periods (run-in, double-blind and washout) did not reveal a change in any measurement except time to onset of angina, suggesting no training effect or change in patient status. Adverse effects were common in patients taking both placebo and bepridil, but only 2 patients had adverse effects (dizziness) with bepridil that necessitated discontinuation of therapy. Similarity of the double product (systolic blood pressure X heart rate) at the end of exercise suggests a decrease in myocardial oxygen demand as the primary mode of action. This study suggests that bepridil is a promising agent for the treatment of exercise-induced myocardial ischemia.

Aged↗

Echocardiographic evaluation of responses to left ventricular volume loading by principal components and nomographic analysis.

Changes in performance of left ventricles (LV) with volume overloads are difficult to determine by conventional clinical methods. This information, however, is important for the proper timing of therapeutic interventions to preserve LV function. Seven size-adjusted (by regression with end-diastolic diameter, EDD) LV performance parameters from 100 normal echocardiograms (echos) were entered into a principal component analysis (PCA). Two factors (linear combination of the 7 parameters) were obtained from the analysis. Prediction limits (95%) about these two factors used in combination, correctly classified 92% of the normal echos. More detailed analysis of the two PCA factors revealed that the majority of the variability within the factors was explained by size-adjusted parameters resultant from the EDD posterior wall (factor 1) and EDD septal excursion (factor 2) regressions, respectively. Plots of the 95% prediction limits about these two regression lines provided nomograms. These nomograms used in combination, correctly classified 95% of the normal echos. When the performance parameters of 64 volume loaded ventricles were evaluated by PCA, four groups were identified. Ten ventricles (16%) were hypokinetic, 29 (45%) were hyperkinetic, 23 (36%) were nomokinetic, and 2 (3%) could not be classified. These classifications were supported by significant between group differences of shortening fraction, velocity of circumferential shortening, and velocity of circumferential expansion. Nomographic classification of the same volume loaded hearts was in excellent (94%) agreement with PCA classification. Nomographic analysis (derived from the PCA) is offered as a less complex, more clinically applicable echo method for evaluating LV performance of volume loaded hearts.

Adolescent↗

Percutaneous transluminal coronary angioplasty in acute myocardial infarction.

Percutaneous transluminal coronary angioplasty (PTCA) has, in general, been restricted to therapy for patients with angina pectoris. Thrombolytic therapy and guide wire recanalization have been used to recanalize coronary arteries in patients with evolving myocardial infarction. Recently we and others have examined the use of PTCA to recanalize the acutely occluded artery associated with the early evolving phase of myocardial infarction. PTCA was performed as definitive therapy in eight patients with acute myocardial infarction. Seven of these had totally occluded arteries to the region of infarct. The infarct-related artery was open within 20 minutes in each of these cases. PTCA recanalization resulted in evidence for reperfusion in each case. Residual stenoses either were not present or were minimal. The procedure was well tolerated. These preliminary results suggest that PTCA may be a reasonable alternative to intracoronary thrombolytic therapy in certain patients with acute evolving myocardial infarction.

Adult↗

Intracoronary streptokinase in evolving acute myocardial infarction.

Intracoronary application of thrombolytic agents, particularly streptokinase, can recanalize arteries that had been totally occluded in patients with evolving acute myocardial infarction (AMI). Numerous uncontrolled trials have testified to the effectiveness of thrombolytic therapy in most patients in reestablishing flow to the infarct-related coronary artery. Follow-up of patients in whom reperfusion has been established has often demonstrated small but significant increases in the left ventricular ejection fraction. In contrast, in other patients in whom thrombolytic therapy failed to reopen the occluded vessel, the left ventricular ejection fraction usually does not change during follow-up. In most reported uncontrolled trials, few complications are described and the mortality rate in patients treated by this therapy may be lower than expected. These data have been used as the basis for widespread application of this technique in many catheterization laboratories around the world. Our initial experience at the University of Florida in 23 patients has not been as successful as other uncontrolled trials previously reported. Reperfusion was accomplished in only 12 patients. Of 17 who survived their AMI, only five demonstrated an improved left ventricular ejection fraction of at least 10%. Serious complications, including bleeding from catheterization sites or allergic reactions to streptokinase, occurred. Controlled trials to critically evaluate this new therapy are needed and are in progress.

Clinical Trials as Topic↗

Intraoperative balloon-catheter dilatation: University of Florida experience.

Thirty-four patients with stable angina underwent coronary artery bypass surgery with supplemental intraoperative coronary artery balloon-catheter dilatation. Coronary dilatation was performed on 35 vessels at 50 sites. The balloon catheter could not be passed through one stenotic site. Intimal dissection occurred at two sites, as noted on early postoperative angiographic studies, with resolution on follow-up studies. There was one perioperative myocardial infarction, 100% early relief of angina, and one operative death. Of 25 distal arterial narrowings studied early by angiography (mean, 10 days), 15 (60%) were unchanged, two (8%) were worse, and eight (32%) were improved. Discrete narrowings improved more than diffuse narrowings; in 46% of the former there was an increase in luminal diameter, in comparison to only 17% of the latter. During a maximal 34-month follow-up period, two patients developed recurrent angina and one died of congestive heart failure. Of 13 distal coronary narrowings studied late (mean, 1 year), six (46%) were unchanged, three (23%) were worse, and four (31%) were improved. Postoperative serial catheterization (early and late) of 10 distal narrowings revealed that nine were unchanged and one was worse. Adjunctive intraoperative coronary balloon-catheter dilatation can be performed safely with acceptable clinical results. The procedure may also allow more complete revascularization of the myocardium.

Angina Pectoris↗

Comprehensive drug management of angina pectoris.

Our current understanding of the pathophysiology of angina and myocardial ischemia includes both anatomic and dynamic mechanisms. The relative contribution made by hemodynamically important atherosclerotic obstruction and dynamic coronary artery obstruction, either by arterial spasm or arteriolar constriction, to the pathophysiology of ischemia in any given patient should be delineated. This information appears to be useful in identifying patients likely to achieve major benefit from vasodilators on the one hand or beta-adrenergic blocking agents on the other. A number of agents are now available within these two pharmacologic classes. There are some differences in action of these various agents that require thorough familiarity of effects of these drugs so that their action can be optimized. Practically speaking, the large majority of patients with an angina syndrome will respond to nitrates. Nitrates are extremely safe and cheap; thus, their use for relief or prevention of the acute ischemic episode remains the initial treatment of choice. When symptoms are more than mild to moderate in severity, or unacceptably controlled in frequency using nitrates alone, other pharmacologic measures are needed (Fig. 2). In patients with a predominant symptom of effort angina, suggesting that a hemodynamically important atherosclerotic-type obstruction is responsible for the syndrome, beta-adrenergic blocking drugs can be very helpful. If effort angina remains unacceptably controlled or adverse effects occur, a calcium-channel antagonist may be added or substituted. These latter agents do not exacerbate bronchospasm or peripheral vascular disease, and they offer a distinct advantage over beta-adrenergic blocking agents in patients with angina who have such disorders. Where the predominant symptom is rest angina, or the patient has other evidence suggesting coronary spasm or arteriolar vasoconstriction, a calcium-channel antagonist may result in a very favorable response. This therapy should be extended not only to patients in whom coronary spasm occurs spontaneously but to those in whom it can be provoked by stimuli such as effort or cold. When spasm is superimposed upon hemodynamically important atherosclerotic obstruction, the favorable response does not seem to be as great as that seen when spasm exists alone. In these cases, coronary bypass surgery, plexectomy , and other nonpharmacologic approaches may have to be added to the pharmacologic regimen.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic beta-Antagonists↗

Role of coronary artery spasm in ischemic heart disease. Therapeutic implications.

The term coronary artery spasm should not be used interchangeably with the specific clinical syndrome "variant angina" since it does occur in other acute and chronic ischemic heart disease syndromes. The term coronary artery spasm should not be applied to patients with ischemic heart disease unless there is clinical, angiographic, and physiologic evidence of its presence. The diagnosis of coronary artery spasm is confirmed by angiography, i.e. change in caliber of the coronary arteries plus evidence of ischemia. Probable diagnosis is in patients who have the syndrome of variant angina, i.e. rest angina associated with ST segment elevation on the electrocardiogram. One can be highly suspicious that the spasm is at work in patients who have rest angina, especially those with unstable angina. One can be suspicious of patients who have variable effort angina or walk-through angina. Coronary artery spasm is a possibility in patients with an acute myocardial infarction or acute re-infarction and is also possible that sudden death in patients with normal coronary arteries can be related to coronary artery spasm. Coronary artery spasm is the usual cause of myocardial ischemia in patients with rest angina without effort angina. This has also commonly been documented in patients with rest and effort angina. There are isolated reports suggesting that patients with effort angina pectoris also develop coronary artery spasm. Coronary artery spasm has been documented to occur in association with acute myocardial infarction. Whether coronary artery spasm is the cause or the result of myocardial infarction has not been determined at this time. However, the recent combined use of intracoronary nitroglycerin and intracoronary streptokinase in patients with acute myocardial infarction has shown reversal of totally obstructed arteries and suggests the relationship between coronary artery disease, coronary artery spasm, and in situ coronary thrombosis. The incidence of sudden death in patients with documented coronary artery spasm is unknown. But, since complete heart block and/or ventricular tachycardia occur during episodes of coronary artery spasm, it is not unreasonable to assume that some patients have died as a result of these rhythm disturbances. The prognosis of patients with coronary artery spasm seems to depend on the presence or absence of severe coronary atherosclerosis, i.e. those with severe disease have a worse prognosis. Current therapy of patients with coronary artery spasm involves the use of nitrates and calcium antagonists.(ABSTRACT TRUNCATED AT 400 WORDS)

Angina Pectoris, Variant↗

Comparison of coronary hemodynamic effects of nitroprusside and sublingual nitroglycerin with anterior descending coronary arterial occlusion.

This study compares the coronary hemodynamic effects of an infusion of nitroprusside and of sublingual nitroglycerin in the same patients. The coronary hemodynamic responses of the anterior left ventricular (LV) region to both drugs were studied in 9 patients whose anterior descending branch of the left coronary artery was filled by collaterals. Before and during administration of each drug (given in doses designed to produce similar changes in LV diastolic pressure), heart rate, LV and aortic pressure, and anterior regional flow, oxygen delivery and lactate metabolism were measured. Given in this manner, as expected, both drugs decreased the double product of heart rate and systolic pressure. Concomitant with these changes, anterior regional blood flow increased or decreased modest amounts or did not change with either drug. Similar directional flow changes or no change occurred in 6 patients and directionally different changes in the other 3 patients. The ratio of mean aortic pressure or of the double product to anterior regional flow consistently decreased during the administration of both drugs. Additionally, anterior regional myocardial oxygen uptake remained similar during both drug periods compared with control values. Anterior region lactate extraction was abnormal (less than 10%) in 4 of the 9 patients during the initial control period. Lactate extraction was usually normal during both the nitroprusside and the nitroglycerin periods. In general, coronary hemodynamic values were remarkably similar during both of these periods. Thus, although relative differences in systemic arterial and venous dilation were obtained with nitroprusside and nitroglycerin, similar and beneficial coronary hemodynamic changes generally occurred.

Aged↗