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Biomedical subjects

W Flameng

Publications and source records attributed to W Flameng.

At least 235 records · Page 13Linked to original sources
PubMed1978

Intraoperative evaluation of the functional significance of coronary collateral vessels in patients with coronary artery disease.

Coronary hemodynamics were studied intraoperatively in 65 patients undergoing aortocoronary bypass grafting. Poststenotic coronary pressure and graft flow hyperemia were measured. Patients without coronary collateral vessels on arteriography (class A) were compared with patients with collateral vessels (class B). Patients in class A were grouped according to the angiographically determined degree of coronary stenosis. Eight of these patients with moderate coronary stenosis underwent intraoperative studies with transient complete coronary occlusion and were classified in the "acute" occlusion group. In class B all patients had complete coronary occlusion with good retrograde filling of the distal segment. In class A patients there was good correlation between the degree of stenosis and poststenotic pressure or hyperemic response. Stenosis had to be at least 80 percent before it produced a significant pressure gradient or graft flow hyperemia. In class B patients (those with complete "chronic" coronary occlusion), poststenotic pressure was significantly greater than in the class A patients with "acute" occlusion, significantly less than in the class A groups with 71 to 80 percent and 81 to 90% stenosis but not significantly different from values in the class A group with 91 to 99 percent stenosis. The hyperemic response was significantly less than in the "acute" occlusion group of class A, significantly greater than in the class A groups with 71 to 80 percent and 81 to 90 percent stenosis, but not significantly different from values in the class A group with 91 to 99 percent stenosis. It is concluded that (1) under basal conditions a coronary stenosis must be at least 80 percent to be hemodynamically significant, and (2) well developed collateral vessels produce in a completely occluded coronary artery hemodynamic changes that simulate those of a 90 percent coronary stenosis without collateral vessels.

Collateral Circulation↗
PubMed1978

[The influence of postischemic reperfusion on the recovery of ischemic lesions of the left ventricle (author's transl)].

In an isolated dog heart preparation the influence of normothermic ischemic arrest and recovery of the ventricular function during the period of post-ischemic reperfusion were investigated. If ischemic arrest has caused a depression of ventricular function, the functional recovery of the myocardium cannot be improved significantly by a prolonged reperfusion of the empty beating heart.

Animals↗
PubMed1978

Recovery from myocardial failure after aortic valve replacement.

Left ventricular hypertrophy and function were studied in 27 consecutive patients with chronic aortic valve disease before and 6.4 +/- 2.2 (S.D.) months after aortic valve replacement with Björk-Shiley prostheses. Four patients were excluded because of postoperative paravalvular regurgitation. Five patients had aortic stenosis (AS), seven patients AS plus insufficiency (AS-AI), and 11 patients aortic insufficiency (AI). Left ventricular muscle mass (LVMI), ejection fraction (EF), mean circumferential fiber shortening rate (VCF), mean normalized systolic ejection rate (MNSER), and peak systolic wall stress (PSWS) were determined angiographically. LVMI fell significantly after corrective surgery, whereas EF, VCF, and MNSER increased. PSWS decreased after the operation. Comparison of stress ventriculograms before and after surgery in six patients with predominant AS (isoproterenol infusion, 0.3 microgram per kilogram of body weight per minute) showed an increase of EF, VCF, and MNSER and a decrease of PSWS. We conclude that hypertrophy in chronic aortic valve disease regresses after aortic valve replacement, and thereby depressed cardiac function and reserve recover.

Adult↗
PubMed1977

[Intraoperative measurements of prognostic value in coronary bypass surgery (author's transl)].

The effect of an aortocoronary bypass graft on coronary hemodynamics was studied experimentally in dogs and during surgery for aortocoronary bypass grafting in man. In the experimental part of this study it was shown that coronary dilatory reserve is unaffected between 0 and 50% coronary narrowing. In the presence of more severe stenosis the dilatory reserve declines rapidly. Competition of flow between an aortocoronary bypass graft and the stenotic segment is related to the degree of coronary stenosis. In 53 patients graft flow was measured during surgery. The relation between hyperemic response (hyperemic/control flow = HR) after short occlusion of the graft and the poststenotic coronary pressure (poststenotic pressure/aortic pressure times 100 = PSPR) could be described by the function HR = a. exp b PSPR (r = 0,87). When the degree of coronary stenosis exceeded 80% narrowing, poststenotic pressure decreased rapidly and hyperemic response appeared. In patients with comparable LAD stenosis a close correlation was found between basal graft flow and anterior wall motion (r = 0,91). It is concluded that graft function can be evaluated by the relation between HR, PSPR and the degree of coronary stenosis. Left ventricular wall motion is shown to be an additional determinant of graft flow.

Animals↗
PubMed1977

Role of cardiac contractility in hypertrophy from chronic volume loading.

In an experimental model of chronic cardiac volume overloading, ie chronic A-V block, evaluations of cardiac function were performed during the phase of the development of hypertrophy (one and two weeks of A-V block) and at stable hypertrophy (ten weeks of A-V block). During a time period of ten weeks of volume overload left ventricular muscle mass increased to 1.41 of normal hearts. Cardiac performance measured from cardiac index, stroke volume, and left ventricular ejection fraction was not depressed at any evaluated state of hypertrophy. Normal cardiac performance was also demonstrated when the heart was stressed by high ventricular pacing rates. The contractile state of the intact heart was expressed as the velocity of the isometric left ventricular pressure rise (dP/dt) at comparable loading conditions. Increased dP/dtmax at a stage before stable hypertrophy was reached, even when preload is normalised by ventricular pacing (70/min) implies that the volume overloaded heart during the development of hypertrophy mobilises part of its contractile reserve. It is assumed that increased contractility is a functional cause of an increase in oxygen demand; and that an adequate energy availability is covered by the enlargement of the mitochondrial mass. At stable hypertrophy when the contractile material has also increased, a new steady state is reached and an again normal contractility indicates an also stable dynamic situation.

Animals↗
PubMed1976

Coronary and contractile reserve in the dog heart with chronic multiple coronary occlusions before and after aortocoronary bypass.

Peak isovolumetric left ventricular pressure and dp/dtmax before and after norepinephrine (N.E.) infusion and cross-clamping of the aorta was identical in normal dogs and in dogs with chronic coronary artery occlusion (C.C.O.) before and after aortocoronary bypass. In normal dogs, coronary reserve was 7.9 and 7.4 times control for the subendocardium and the subepicardium. After C.C.O., coronary reserve was 7.0 and 5.7 times control in the normal area and 2.4 and 3.5 times control in the collateral dependent area (endo vs. epi). After N.E. myocardial blood flow increased to 57% of the coronary reserve in normal dogs, and to 100% in dogs with C.C.O. After bypass, myocardial blood flow normalized. In dogs with C.C.O., N.E. stimulated the contractile reserve maximally and the coronary reserve is completely expended.

Animals↗
PubMed1976

Vascular and cardiac contractile reserve in the dog heart with chronic multiple coronary occlusions.

Nineteen mongrel dogs survived chronic occlusion of the left circumflex and of the right coronary artery without infarction due to the timely development of a collateral circulation. Only 38 per cent of the conductance of the arteries before occlusion was restored by collateral vessels. In these animals and in 15 control dogs with normal coronary arteries myocardial contractility, contractility reserve, and myocardial blood flow were studied. The same was done in dogs with chronic coronary artery occlusion after aortocoronary bypass. Myocardial blood flow was determined woth the tracer microsphere technique. Contractility reserve was tested and defined as isovolumetric left ventricular pressure and dp/dt max with norepinephrine infusion and cross-clamping of the aorta. Contractile reserve was not significantly different between normal dogs and dogs with chronic coronary artery occlusion before and after aortocoronary bypass. Myocardial blood flow during control conditions was homogenously distributed in all three groups studied. The ratio of blood flow to the endocardium and the epicardium was not significantly different from inity. Coronary reserve was determined at peak reactive hyperemia following a 20 second period of coronary artery occlusion, with ongoing norepinephrine infusion. Under these conditions subendocardial fow in normal dogs rose by a factor of 7.9 while subepicardial flow increased 7.4 times. In dogs with chronic occlusion of two coronary arteries the increase of myocardial flow was nonnomogenous; subendocardial flow to areas supplied by a normal coronary artery rose by a factor of 7.0 while subepicardial flow increased 5.7 times control. Subendocardial collateral flow rose by a factor of 2.4 and subepicardial collateral flow increased 3.5 times control. In normal dogs norepinephrine alone did not result in maximal coronary flow but only 57 per cent thereof. Dogs with chronic coronary occlusion, however, required the entire coronary reserve in areas that were supplied by a normal coronary artery, whereas areas supplied by collaterals became ischemic. Opening of an aortocoronary bypass restored normal flow to previously ischemic areas, and reduced the flow to areas supplied by a normal artery. With the bypass open no differences existed between normal dogs and those with two occluded coronary arteries. We conclude that the norepinephrine-stimulated contractile reserve of hearts with chronic coronary occlusion was comparable to that of normal hearts; however, norepinephrine forced these hearts to spend the entire flow reserve of the remaining normal artery while producing ischemia in collateral-dependent areas. The same dose of norepinephrine did not require the entire flow reserve of normal dogs.

Animals↗
PubMed1976

[Early experiences with arterial heterografts (author's transl)].

Since April 1975 we used 50 bovine arterial heterografts for reconstructive surgery after chronic arterial occlusions or for the production of AV-shunts needed for chronic dialysis. In none of the cases incompatibility was seen. The early results (with a follow-up period of 6-10 months) after femoro-popliteal bypass were excellent, as far as a good peripheral run off was present. Several shunts (n = 7) containing 2-3 transplants, are still functioning 3-10 months after implantation. At present, we use bovine transplants in reconstructive vessel surgery when a thrombendarterectomy or the connection of venous grafts is impossible or when the operative procedure should be kept short in high-risk patients. To produce AV-shunts in patients with renal insufficiency we prefer this type of grafts when all conventional techniques were already used.

Animals↗
PubMed1976

[Early and late complications due to direct and indirect aortic-isthmus-Plastic (author's transl)].

During the last 20 years 156 patients underwent a direct and indirect aortic-isthmus-plastic. Early complications occurred in 7.6%. 5 patients developed an aneurysm in the area of isthmus-plastic. The mortality rare was 4.5%. There was no evidence of recurrent coarctation in a group of children and in adult patients. The indirect aortic-isthmus-plastic first described by Vosschulte represents an elegant surgical method of functionally reestablishing the aortic lumen by retaining the posterior wall for further growth potential. This technique can be performed with a low mortality rate and no recurrent coarctation of the aorta.

Adolescent↗
PubMed1976

Quantification of collateral resistance in acute and chronic experimental coronary occlusion in the dog.

The resistance to coronary blood flow in various parts of the myocardium was studied with the tracer microspheres technique before and immediately after an acute coronary occlusion and several weeks after a more slowly occurring coronary occlusion by Ameroid constrictor. All experiments were carried out in the isolated, metabolically supported, empty, beating dog heart at maximal coronary vasodilation induced with adenosine. Coronary resistance of the normal empty beating heart at maximal coronary vasodilation was 0.20 mm mm Hg/(ml/min) per 100 g of tissue (subepicardium) and 0.16 mm Hg/(ml/min) per 100 g of tissue (subendocardium). After acute coronary occlusion the perfusion of the subtended myocardium was maintained at a much lower level by way of collateral vessels, which showed a resistance to flow of 3.52 mm Hg/(ml/min) per 100 g. If coronary artery occlusion proceeded more slowly the collateral vessels became more functional and myocardial infarction was avoided. During collateral enlargement collateral resistance fell from 3.52 to 0.22 mm Hg/(ml/min) per 100 g within a period of 8 weeks after implantation of the constricting device. The degree of compensation by collaterals for the loss of the occluded native coronary artery was 33% of its former conductance.

Acute Disease↗
PubMed1975

Influence of perfusion pressure and heart rate on local myocardial flow in the collateralized heart with chronic coronary occlusion.

We studied the influence of controlled changes in perfusion pressure and heart rate on the regional distribution of myocardial flow in normal dogs and in dogs with multiple chronic coronary artery occlusions but without infarctions. Local myocardial blood flow was determined with the tracer microsphere technique. By stepwise altering of systemic blood pressure during maximal vasodilation classical pressure flow relations were obtained. One week after complete chronic occlusion a functionally and anatomically well-defined compartmentation of blood flow was found. The dilatory reserve is clearly compromised not only in the collateral-dependent myocardium but also in the apparently normal myocardium which delivers collateral flow. An "arterio-arterial shunting" mechanism is shown to exist. Several months after coronary occlusion, regional mycoardial flow is still nonhomogeneous. Although the coronary dilatory capacity of the collateralized myocardium is nearly normal, that of the normal myocardium is found to be higher than normal. Vessel growth in both areas is discussed as being responsible for this phenomenon. Right ventricular pacing during maximal vasodilation produces a flow decrease to the endocardial muscle layers in normal dogs, while the epicardial flow is unchanged. One week after complete chronic coronary occlusion pacing during maximal vasocilation reduces the dilatory capacity in the collateralized areas to such an extent that the supplementary increase in myocardial oxygen demand will induce ischemia because of the compromised oxygen supply.

Animals↗
PubMed1975

[Effect of intraaortic-ballon-counterpulsation on the changes of myocardial blood flow following coronary artery stenosis and occlusion (author's transl)].

To prove the effectiveness of the IABP in case of impending myocardial infarction in one series of experiments myocardial blood flow changes due to IABP in dogs with stenosis of the left circumflex coronary artery (LC) were investigated using tracer microspheres. In a control series the left anterior descending artery (LAD) was occluded. In acute LAD occlusion the IABP caused an increase of blood flow in the epicardial layer. In case of LC stenosis there was a far greater increase in blood flow by the IABP most prominent in the endocardial layer. Our experiments indicate that the IABP seems to be effective in impending myocardial infarction.

Animals↗