Biomedical subjects
Publications and source records attributed to C R Conti.
A quantitative coronary arteriographic technique is described utilizing 105-mm photospot angiography and a hand-held optical magnifying device. This technique is rapid, accurate, and reproducible. We feel this technique has potential in evaluating coronary responses to acute interventions and in the long term evaluation of progression or regression of atherosclerotic disease.
Arterilization of the coronary venous system has been suggested as a means of myocardial perfusion. We recently studied a patient with a saphenous vein aorto=coronary venous bypass graft created inadvertently during surgery intended to bypass the anterior descending artery. We selectively injected onctrast into this graft during balloon occlusion of the coronary sinus both before and after sublingual nitroglycerin. No arterial visualization was demonstrated from the vein and no evidence to suggest perfusion of the myocardium was found.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The clinical and prognostic significance of the direction of the S-T segment shift on the 12-lead electrocardiogram was evaluated in medically treated patients with unstable angina pectoris. Long-term mortality and morbidity of 11 patients with transient S-T segment elevation (group I) were compared to that of 21 patients with transient S-T segment depression (group II). The average follow-up duration was 62 months. There was no significant difference between groups I and II with respect to survival or nonfatal myocardial infarction over a five-year period. Mortality was related to the extent of coronary artery disease and left venticular ejection fraction rather than to the direction of the S-T segment shift.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The haemodynamic effects of oral prazosin and hydralazine were evaluated in patients with refractory heart failure and compared with those of intravenous nitroprusside in the same patients. Both oral agents were well tolerated and appeared to have beneficial haemodynamic effects. Prazosin and hydralazine produced similar increases in cardiac output associated with a similar decrease in systemic vascular resistance. Prazosin and hydralazine produced similar increases in cardiac output associated with a similar decrease in systemic vascular resistance. Prazosin resulted in a more significant decline in left ventricular filling pressure and pulmonary vascular resistance than did hydralazine. Haemodynamic alterations induced by prazosin were similar to those induced by nitroprusside, which suggests a relatively balanced reduction of preload and afterload. With hydralazine, the increase in cardiac output without change in left ventricular filling pressure or pulmonary vascular resistance suggests minimal effect on preload but significant reduction in afterload.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In summary, it is hazardous to rely solely on coronary angiography to define critical coronary stenosis. Clinically, the physiologic significance of a narrowing observed at coronary angiography can best be evaluated by obtaining additional evidence of myocardial ischemia, i.e. stress testing with ECG monitoring, resting and exercise isotope perfusion studies or ventriculographic studies. However, when evaluating coronary angiograms for critical coronary stenosis, several points are worth considering. First, a long narrowing will decrease coronary blood flow more than a short narrowing of the same severity. Second, sequential narrowings will decrease coronary blood flow more than a single narrowing of the same total length. Third, a long narrowing can be estimated more accurately than a short narrowing. Fourth, caliper measurements of coronary artery narrowings are more accurate than subjective estimation, and fifth, coronary artery dilators may increase the percentage narrowing in some cases. The complex effects of percent stenosis and length of stenosis on the physiology of coronary blood flow must always be considered when evaluating angiograms. In addition, the angiographic or photographic artifacts produced by short narrowings tend to overestimate the percent stenosis and, thus, calipers should be used to measure percent stenosis, especially in the short narrowings.
Explore the source record for details and available documents.
Ergonovine has been shown to provoke attacks of variant angina, but a question remains whether spontaneous and ergonovine-induced attacks of variant angina are similar. Seven patients with variant angina undergoing cardiac catheterization were studied during transient episodes of spontaneous and ergonovine-induced rest angina with ST-segment elevation. Clinical, electrocardiographic, left ventricular hemodynamic and coronary angiographic observations were made before and repeated after ergonovine (0.05-0.2 mg I.V.). The character and duration of chest pain were similar during both spontaneous and ergonovine-induced episodes. ST-segment elevation (greater than 1 mm) was present inferiorly in three patients, anteriorly in three patients, and both inferiorly and anteriorly in one patient during both episodes. Mean heart rate and systolic arterial pressure changed little, while left ventricular end-diastolic pressure increased significantly during spontaneous or ergonovine-induced attacks. We observed subtotal or total dynamic obstruction in the left anterior descending (three patients), right coronary arteries (three patients) and both arteries in one patient during both attacks. Thus, in selected patients ergonovine-induced attacks of variant angina were remarkably similar to spontaneous episodes.
The coronary hemodynamic effects of controlled aortic insufficiency (AI) were studied in 10 dogs. Coronary blood flow (CBF), before and during reactive hyperemia (RH) with graded coronary diameter narrowings (CN), aortic (Ao) and left ventricular (LV) pressures (P), and aortic blood flow (AoF) were recorded. Opening an adjustable basket catheter, positioned across the aortic valve, created reversible AI quantitated from phasic AoF. AI was regulated so that mean CBF was similar with or without AI. During AI, heart rate and systolic AoP were unchanged, but diastolic AoP declined 14 mm Hg (mean) and end-diastolic LVP increased 8 mm Hg, both p less than 0.05. With CN greater than or equal to 85%, mean CBF decreased with or without AI. Coronary resistance was similar with or without AI. During AI with no CN, peak RH CBF declined significantly and was similar to peak RH with 70% CN without AI. Furthermore, AI with 60% CN caused additional reduction in peak RH and was similar to peak RH with 80% CN without AI. These data suggest that CBF reserve, exposed during RH, is decreased during AI. With AI, a given CN has coronary hemodynamic properties similar to higher degrees of CN without AI. These results may relate to clinical findings of ischemia in patients with AI and no or moderate CN.
Beneficial effects of nitroprusside infusion in heart failure are purportedly a result of decreased afterload through "impedance" reduction. To study the effect of nitroprusside on vascular factors that determine the total load opposing left ventricular ejection, the total aortic input impedance spectrum was examined in 12 patients with heart failure (cardiac index <2.0 liters/min per m(2) and left ventricular end diastolic pressure >20 mm Hg). This input impedance spectrum expresses both mean flow (resistance) and pulsatile flow (compliance and wave reflections) components of vascular load. Aortic root blood flow velocity and pressure were recorded continuously with a catheter-tip electromagnetic velocity probe in addition to left ventricular pressure. Small doses of nitroprusside (9-19 mug/min) altered the total aortic input impedance spectrum as significant (P < 0.05) reductions in both mean and pulsatile components were observed within 60-90 s. With these acute changes in vascular load, left ventricular end diastolic pressure declined (44%) and stroke volume increased (20%, both P < 0.05). Larger nitroprusside doses (20-38 mug/min) caused additional alteration in the aortic input impedance spectrum with further reduction in left ventricular end diastolic pressure and increase in stroke volume but no additional changes in the impedance spectrum or stroke volume occurred with 39-77 mug/min. Improved ventricular function persisted when aortic pressure was restored to control values with simultaneous phenylephrine infusion in three patients. These data indicate that nitroprusside acutely alters both the mean and pulsatile components of vascular load to effect improvement in ventricular function in patients with heart failure. The evidence presented suggests that it may be possible to reduce vascular load and improve ventricular function independent of aortic pressure reduction.
Although the motion of the left ventricular wall has been examined by angiographic and by echocardiographic studies in both experimental animals and in man, there are no complete studies of the motion of the left ventricular posterior wall throughout the entire cardiac cycle. Because the posterior wall can be demonstrated echocardiographically in essentially all patients, it offers a potential of wide clinical application in the evaluation of left ventricular function. This study was undertaken to provide a detailed inclusive analysis of the motion of the left ventricular posterior wall. In 64 human volunteers the echocardiographic movements of the left ventricular posterior wall were identified. Using the R wave of the electrocardiogram as a reference and to identify phases of the cardiac cycle, each movement of the left ventricular posterior wall was temporally related to aortic or mitral valvular movements (or both). In a subset of 14 subjects, dual M-mode echocardiograms confirmed the validity of these temporal relationships. In three subjects, high-fidelity recordings from catheter tip micromanometers were made simultaneously with the echocardiogram to permit description of the temporal relationships between pressure and motion. Results of this study provide a base of normal data for comparison with the motion of the left ventricular posterior wall in a variety of diseases and in response to therapy.
Although considerable investigation has been devoted to the concept of "critical" coronary stenosis, there is general lack of agreement on which coronary stenoses consistently decrease coronary blood flow (CBF). In 32 open-chest dogs we studied CBF and the aorta-distal coronary pressure gradient at rest and with reactive hyperemia (RH) as stenoses were created in the left coronary artery (LCA) or its major branches--anterior descending (LAD) or circumflex (LCx) arteries. The effects of stenosis location, reduction in stenosis diameter, stenosis length, and the number of stenoses were studied. Resting CBF and resting distal coronary pressure were decreased by short snare stenoses, which reduced the diameter of the LCA or either major branch more than 80%. Lengthening 50 to 60% LAD or LCx stenoses decreased CBF and increased the pressure gradient. There were small increases in pressure gradients but no change in CBF with multiple stenoses in either the LAD or LCx branch. During peak RH, CBF was decreased by a 60% LCA or branch snare stenosis. Peak RH CBF responses decreased further as length of an LAD or LCx stenosis increased. Multiple stenoses affected peak RH CBF responses significantly more than a single stenosis of the same total length. These data indicate that several anatomic variables of coronary stenosis affect the physiological responses of the coronary circulation. The variables are (1) reduction in lumen diameter, (2) length of stenosis, and (3) number of stenoses in one vessel.
Explore the source record for details and available documents.