Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CORONARY VESSELS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources
PubMed1992

A comparison of angioplasty with medical therapy in the treatment of single-vessel coronary artery disease. Veterans Affairs ACME Investigators.

BACKGROUND: Despite the widespread use of percutaneous transluminal coronary angioplasty (PTCA), only a few prospective trials have assessed its efficacy. We compared the effects of PTCA with those of medical therapy on angina and exercise tolerance in patients with stable single-vessel coronary artery disease. METHODS: Patients with 70 to 99 percent stenosis of one epicardial coronary artery and with exercise-induced myocardial ischemia were randomly assigned either to undergo PTCA or to receive medical therapy and were evaluated monthly. The patients assigned to PTCA were urged to have repeat angioplasty if their symptoms suggested restenosis. After six months, all the patients had repeat exercise testing and coronary angiography. RESULTS: A total of 107 patients were randomly assigned to medical therapy and 105 to PTCA. PTCA was clinically successful in 80 of the 100 patients who actually had the procedure, with an initial reduction in mean percent stenosis from 76 to 36 percent. Two patients in the PTCA group required emergency coronary-artery bypass surgery. By six months after the procedure, 16 patients had had repeat PTCA. Myocardial infarction occurred in five patients assigned to PTCA and in three patients assigned to medical therapy. At six months 64 percent of the patients in the PTCA group (61 of 96) were free of angina, as compared with 46 percent of the medically treated patients (47 of 102; P less than 0.01). The patients in the PTCA group were able to increase their total duration of exercise more than the medical patients (2.1 vs. 0.5 minutes, P less than 0.0001) and were able to exercise longer without angina on treadmill testing (P less than 0.01). CONCLUSIONS: For patients with single-vessel coronary artery disease, PTCA offers earlier and more complete relief of angina than medical therapy and is associated with better performance on the exercise test. However, PTCA initially costs more than medical treatment and is associated with a higher frequency of complications.

Adrenergic beta-Antagonists↗
PubMed1980

'Variant' angina: evidence for small vessel coronary artery spasm?

A unique case of 'variant' angina pectoris has been observed in a patient with normal coronary arteries and typical chest pain appearing spontaneously at rest, and repeatedly provoked by ergonovine maleate (0.1 mg iv) associated with large transmural perfusion defects on 201Tl-imaging (after ergonovine) and a marked increase in T wave voltage despite no demonstrable spasm of a major coronary artery after the same doses of ergonovine. While saline solution could not provoke chest pain and treatment with a beta-blocking agent increased the frequency of ischemic attacks, a calcium antagonist therapy reduced and eventually eliminated the attacks. Thus, this case provides evidence for yet another aspect of a 'variant' form of angina pectoris: small vessel coronary artery spasm.

Adult↗
PubMed2004

Feasibility and cost of treatment with drug eluting stents of surgical candidates with multi-vessel coronary disease.

OBJECTIVE: To determine the feasibility and cost of treatment with drug eluting stents in patients with multi-vessel coronary disease referred currently for surgical revascularisation. METHODS: Two experienced interventional cardiologists reviewed retrospectively the clinical records and pre-operative coronary angiograms of 209 patients who underwent their first coronary bypass operation for multi-vessel disease without other adjunctive surgical procedures at the Royal Brompton Hospital in 2002. They were classified according to the technical feasibility and completeness of percutaneous revascularisation. A cost decision-analysis model with a cost of drug eluting stents of euro 2,100 and simulated 1-year costs was constructed. RESULTS: Mean age was 64.6+/-8.9 years with 54 diabetics (25.8%). Each patient received at least 1 arterial graft and a mean of 3.0+/-0.8 distal anastomoses. Mean post-operative stay was 8.9+/-7.2 days and total cost euro 19,821+/-1,964. Percutaneous revascularisation was judged to be feasible in 158 (76%) cases. The contraindications were at least 1 unfavourable total occlusion subtending viable myocardium in 48 patients (23%) and extreme tortuosity or calcification in 4 patients (2%). Percutaneous revascularisation of grafted major epicardial vessels was anticipated to be complete in 138 (66%) patients and partial but acceptable in 19 (9.1%) patients. Stenting of the left main, of a 'favourable' total occlusion, of bifurcations or in an ostial location would have been required in 32 (20.4%), 60 (38.2%), 77 (49.0%) and 74 (47.1%), respectively, of cases treated. 3.6+/-1.4 drug eluting stents of total length 72.6+/-37.3 mm were required to treat 3.3+/-1.2 lesions per patient at an estimated cost of euro 17,266+/-2,850. When one year repeat revascularisation was modelled at a rate of 15% in the stent group there was no significant cost saving from stenting. CONCLUSIONS: Although percutaneous revascularisation is feasible in 76% of patients currently undergoing coronary artery bypass grafting for multi-vessel disease, such an approach will involve frequent treatment of complex lesions for which no long term results are available and is unlikely to provide appreciable economic savings.

Aged↗
PubMedDate not supplied

The relation between chronic obstructive pulmonary disease and coronary collateral vessels.

Coronary collateral vessels can provide a perfusion reserve in case of increased myocardial oxygen demand. Development of coronary collateral vessels (CCV) is triggered by the pressure gradient between the coronary bed of arteries caused by an obstruction and myocardial ischemia. Myocardial hypoxia can facilitate development of CCVs. There is a chronic hypoxemia in patients with chronic obstructive pulmonary disease (COPD). The aim of this study was to evaluate the effect of COPD on CCVs. The study included 98 patients with COPD who underwent coronary angiography. Those patients in whom coronary angiography is normal or severity of coronary artery stenosis in thought not to be sufficient for the development of CCVs (<80%) were excluded from the study. A total of 98 patients (mean age, 62 +/-9 years) met the criteria for the COPD group. For case-control matching, 98 consecutive without COPD patients (mean age 62 +/-10) who had one or more diseased vessels with 80% or greater stenosis were included in the control group. The CCVs were graded according to the Rentrop scoring system, and the collateral score was calculated by summing the Rentrop numbers of every patient. The mean number of diseased vessels in patients with COPD and without COPD were 1.61 +/-0.69 and 1.77 +/-0.89 (p=0.155), respectively. The mean collateral score was 2.15 +/-2.03 in the COPD group and 1.32 +/-1.54 in the control group. After confounding variables were controlled for, the collateral score in patients with COPD group was significantly different from that in patients without COPD group (p=0.002). These findings suggest that CCV development is better in patients with COPD than in those patients without COPD. Thus, COPD may be an important factor affecting CCV development, which may be related to the presence of chronic hypoxemia in patients with COPD.

Aged↗
PubMed2002

Catecholaminergic nerve fibers and beta-adrenergic receptors in the human heart and coronary vessels.

The relationship between catecholaminergic nerve fibers and beta-adrenergic receptors in the heart and in the coronary vessels was studied in humans. Only living tissues, harvested from brain-dead heart donors, were used in this experiment. Morphological observations and histochemical staining for norepinephrine and other catecholamines were carried out and beta-adrenergic receptors were stained by means of a beta-blocking fluorescent drug. All morphological data underwent quantitative analysis of images and statistical evaluation. This study provided direct evidence for the distribution of catecholaminergic nerve fibers and of beta-adrenergic receptors in the myocardium and in the coronary arteries. Catecholaminergic nerve fibers are located in the periadventitial tissue, in the adventitia and in the transitional zone between the intima and media. The beta-adrenergic receptors are mainly located in the more innervated part of the heart and coronary arteries but there is a major, although incomplete, overlap with related catecholaminergic nerve fibers. Moreover, using specific substrates and/or inhibitors, two types of beta-adrenergic receptors, beta(1) and beta(2), were demonstrated. Owing to the scarcity of available material (we used only four hearts), and objective difficulties in enrolling other patients, we are at this moment unable to draw general conclusions.

Adult↗
PubMed2002

Role of VEGF family members and receptors in coronary vessel formation.

The specific roles of vascular endothelial growth factor (VEGF) family members and their receptors (VEGFRs) in coronary vessel formation were studied. By using the quail heart explant model, we found that neutralizing antibodies to VEGF-B or VEGF-C inhibited tube formation on the collagen gel more than anti-VEGF-A. Soluble VEGFR-1, a receptor for VEGF-A and -B, inhibited tube formation by 87%, a finding consistent with that of VEGF-B inhibition. In contrast, addition of soluble VEGFR-2, a receptor for VEGF family members A, C, D, and E, inhibited tube formation by only 43%. Acidic FGF-induced tube formation dependency on VEGF was demonstrated by the attenuating effect of a soluble VEGFR-1 and -2 chimera. The localization of VEGF R-2 and R-3 was demonstrated by in situ hybridization of serial sections, which documented marked accumulations of transcripts for both receptors at the base of the truncus arteriosus coinciding with the temporal and spatial formation of the coronary arteries by means of ingrowth of capillary plexuses. This finding suggests that both VEGFR-2 and R-3 may play a role in the formation of the coronary artery roots. In summary, these experiments document a role for multiple members of the VEGF family and their receptors in formation of the coronary vascular bed.

Animals↗
PubMed2003

Transmitral pulsed-Doppler echocardiography is a more accurate technique compared with two-dimensional echocardiography using dobutamine, in patients with one vessel coronary artery disease.

UNLABELLED: To examine the effects of dobutamine on pulsed-Doppler left ventricular filling indices and its utility for evaluation of CAD we studied 14 patients with normal coronary arteries (Group 1) and 39 patients with significant CAD (>70% diameter stenosis). Patients with coronary artery disease (CAD) were divided into two groups: patients with one-vessel coronary disease (Group 2); and those with multivessel CAD (Group 3). After stopping cardioactive treatment, patients underwent incremental dobutamine stress (5, 10, 20, 30 and 40 microg/kg/min) during pulsed-Doppler interrogation of diastolic filling with simultaneous heart rate and blood pressure measurements. The following transmitral Doppler variables were measured at baseline and at peak-dose of dobutamine: peak early (E) and peak atrial (A) velocity; E/A ratio; acceleration time (AT) and deceleration time (DT) of E wave; isovolumic relaxation time (IVRT); and time-velocity integral (TVI). Two-dimensional echocardiography was performed to detect regional asinergy and analyzed using a 16 segment model. RESULTS: Normals and CAD patients showed comparable changes in heart rate and blood pressure (P=NS between groups). Intergroup analysis of the changes of transmitral flow showed the significant changes for these indices (P<0.001): E velocity (-2.78+/-10.04, 12.4+/-9.4 and 16.47+/-10.65 cm/s); AT of E wave (1.66+/-2.47, -5.2+/-1.38 and -4.66+/-2.39 m/s(2)); DT of E wave (-0.23+/-0.18, 0.2+/-0.2 and 0.2+/-0.28 m/s(2)); and TVI of transmitral flow (-1.26+/-0.7, 3.5+/-1.75 and 4.1+/-1.66 cm), respectively for Groups 1, 2 and 3. All other transmitral Doppler variables showed insignificant changes (P=NS) to dobutamine between groups. It is important that the significance of these changes were the same for patients with one-vessel and those with multivessel coronary disease. In conclusion, during dobutamine stress testing, patients with CAD, had an abnormal response of these transmitral Doppler indices: E wave; AT of E wave; DT of E wave; and the TVI of transmitral flow. The abnormal responses of these Doppler indices of left ventricular filling are more accurate markers of significant single vessel CAD than new wall motion abnormalities during conventional DSE.

Adrenergic beta-Agonists↗
PubMed1985

Positive treadmill stress tests post myocardial infarction in patients with single-vessel coronary disease.

To investigate the possibility that patients with single-vessel coronary artery disease (CAD) and recent myocardial infarction (MI) can have ST segment depression on post infarction treadmill testing due to ischemia, we studied 16 such patients who underwent cardiac catheterization and exercise testing after MI. Of the 11 patients with ST segment depression on treadmill testing, 10 failed to increase their ejection fraction and nine had a focal worsening of wall motion during exercise radionuclide ventriculography. Seven of these 11 patients had hypokinesis or normokinesis in the suspected area of infarction. In contrast, four of the five patients without ST segment depression on treadmill stress testing had an increase in ejection fraction with stress which was significantly greater than that seen in patients with ST depression (7.2% vs 0%, p less than 0.05). Short-term follow-up (1.1 years) revealed continued post infarction angina in 10 of the 11 patients with positive treadmill stress tests. Four of these patients underwent either percutaneous transluminal angioplasty or surgery. We conclude that positive post infarction treadmill tests due to exercise-induced ischemia may occur in patients with single-vessel CAD and may be associated with continued angina that requires surgical intervention.

Adult↗
PubMed1989

[Morphologic changes of the coronary vessels in patients with congenital heart defects].

Results of the study of the structural changes in the coronary vessels at various levels of ramification in patients with heart defects are presented and their role in the heart compensation and decompensation is shown. 127 hearts with congenital defects and 45 control children's hearts were studied. It is established, by means of anatomical, histologic and morphometric methods, that the heart defects are followed by the hypertrophy of the heart regions involved functionally, this being combined with an adaptive and pathologic rearrangement of coronary arteries and veins. The former is expressed in the vessels hyperplasia, thickening of their wall, and in the appearance in the vascular wall of oblique and longitudinal smooth myocytes (this is of importance for the maintenance of the heart compensation state). The latter is manifested in sclerosis, sometimes also thrombosis of the coronary arteries and veins this creating the basis for the heart failure.

Cardiomegaly↗
PubMed1992

[Two-phase effect of endothelin-1 on resistance of coronary vessels in anesthesized rats with intact chest].

Effects of intracoronary infused (2 pM/kg/min for 5 min) endothelin-I on coronary blood flow was studied using modification of the method of Vetterlein and Schmidt. Blood flow in extracorporeal circuit was measured by 20 MHz pulsed Doppler flowmeter. One end of the circuit was connected to the left common carotid artery and the other was connected to the especially curved glass cannule which was placed to the origin of the coronary artery and through the right common carotid artery. Five-minute infusion of endothelin was followed by transitory dilatation and then by constriction of coronary vessels. Blockade of dihydropyridine-sensitive Ca-channels potentiated endothelin-induced vasodilation and decreased the constrictor response three-fold.

Animals↗
PubMed1981

Complex ventricular arrhythmias after myocardial infarction during convalescence and follow-up: a harbinger of multi-vessel coronary disease, left ventricular dysfunction and sudden death.

Sixty-one medically treated patients had coronary and left ventricular angiography and 24-hour electrocardiographic monitoring 10-24 days after myocardial infarction, and then had serial 24-hour electrocardiographic monitoring during the 13 +/- 11 months after myocardial infarction. Complex ventricular arrhythmias (2 or more sequential ventricular premature depolarizations (VPDs), multiform VPDs, bigeminy) during follow-up were associated with a high mortality rate and occurred most commonly in the setting of three-vessel coronary disease, proximal left anterior descending coronary disease and low left ventricular ejection fraction. By contrast, patients without complex VPDs in either the late hospital or posthospital phase of myocardial infarction had no mortality during the year following myocardial infarction; furthermore, these patients had a higher incidence of single-vessel coronary disease and less left ventricular dysfunction. These results emphasize the adverse prognostic significance of complex ventricular arrhythmias in the year after myocardial infarction and their association with extensive coronary artery disease and left ventricular damage.

Arrhythmias, Cardiac↗
PubMedDate not supplied

Coronary vessel alterations following chronic carbon monoxide exposure in the adult rat.

Adult male rats were exposed to 500 ppm CO continuously for 30 days, while litter-mate controls remained in room air (AIR). Heart weight-to-body weight ratio and hematocrit were increased significantly. Right ventricle (RV) free wall thickness was increased significantly as was right to left heart diameter and average heart diameter. Cross-sectional areas of the left ventricle (LV) free wall, interventricular septum (S) and RV midway between the apex and base were increased significantly. Morphometric analysis of the CO-exposed and AIR hearts revealed no significant differences in the number of small (27-114 microns) or larger (> 114 microns) blood vessels in any region; however, there was a trend towards an increased number of the smaller vessels, both arterioles and venules, in the CO-exposed rats. The larger arteries in the S and RV were significantly larger in the CO-exposed rats. There was a significant overall effect of CO on larger artery diameter across all heart regions, consistent with the appearance of heart radiographs taken. There were no differences in the diameter of the small vessels in any region of the heart between the CO-exposed and AIR rats. The vessel cross-sectional area of the larger vessels tended to be increased in all regions of the heart. The cross-sectional area of the large arteries in the LV was increased significantly. Arterial wall thickness was decreased significantly in RV and there was a significant overall effect of CO in decreasing wall thickness and the ratio of wall thickness-to-vessel luminal diameter in these vessels. No vascular pathology was observed. The results of this study suggest changes in coronary vessel architecture during chronic CO-induced cardiac hypertrophy and are consistent with earlier hemodynamic and morphometric studies of CO-exposed hearts.

Animals↗
PubMed2001

Acute and long-term outcomes of stenting in coronary vessel > 3.0 mm, 3.0-2.5 mm, and < 2.5 mm.

We compared the acute and long-term outcomes of stentings in coronary vessels > 3.0 mm, 3.0-2.5 mm, and < 2.5 mm. A total of 1,152 patients underwent coronary stenting was divided into three groups based on the reference vessel size. Group A consisted of 598 patients (667 lesions) with a reference vessel diameter > 3.0 mm, group B 485 patients (544 lesions) with a reference vessel diameter of 3.0-2.5 mm, and group C 114 patients (119 lesions) with a reference vessel diameter < 2.5 mm. The procedural success, stent thrombosis, and in-hospital cardiac event rate were similar in the three groups. At 6-month angiographic follow-up, the lesion restenotic rate was significantly higher in the small-vessel group (14%, 22%, and 26% in groups A, B, and C, respectively; P = 0.011). These differences appeared to result from a lesser acute gain and a lesser net gain in small-vessel group; the late luminal loss was similar in the three groups. During a follow-up duration of 28 +/- 3 months, group C patients had a significantly lower rate of event-free survival than the group A and B patients (71% vs. 85% and 82%; P = 0.002). Stepwise regression analysis demonstrated that complex lesion (P = 0.032) and long lesion (P = 0.046) are independent predictors of restenosis in very-small-vessel (< 2.5 mm) stenting. In conclusion, the acute results of stenting in small coronary arteries appear safe and feasible with a high procedural success rate and a low incidence of stent thrombosis. Stenting in patients with a small coronary artery appears to have a similar in-hospital cardiac event rate, but a higher angiographic restenosis rate and a lower event-free survival rate, compared to stenting in patients with a larger coronary artery. The predictors of restenosis in very-small-vessel stenting are complex lesions and long lesions. Cathet Cardiovasc Intervent 2001;53:314-322.

Aged↗
PubMed1985

[Dilatation of epicardial coronary vessels by intravenous diltiazem in patients with coronary heart disease].

UNLABELLED: Coronary diameters and central hemodynamics were measured in 22 patients with stable coronary artery disease before and after 20 mg of intravenous diltiazem. Coronary diameters from high quality biplane coronary angiograms were calculated as mean values after caliper measurements of identical segments. Measurements were made in angiographically normal and abnormal proximal, middle and distal vessel segments. Central hemodynamics showed a significant decrease for heart rate, mean aortic pressure and peripheral resistance (p less than 0.001). Coronary diameters increased between 2 and 16% (proximal or distal segments). Diameter increases were statistically significant for all segments (p less than 0.001) except for proximal atherosclerotic segments. These hemodynamic and diameter changes were seen after 5, 10 and 20 minutes. CONCLUSION: Intravenous diltiazem shows an acute coronary dilative effect in patients with stable coronary artery disease. This effect is regarded as one of the essential antianginal actions of the drug.

Benzazepines↗
PubMed1987

Media hypertrophy in hypertensive coronary resistance vessels.

Coronary reserve is reduced in human hypertensive hypertrophy and in the model of spontaneously hypertensive rats (SHRs). In isolated coronary resistance vessels, the role of structural and functional changes was evaluated. Furthermore, the effect of long-term antihypertensive therapy was also studied. At the age of 20 weeks, SHR and Wistar-Kyoto (WKY) rats were examined. Distal segments of the left anterior descending coronary artery were dissected and mounted on a myograph developed by Mulvany and Halpern. After recording of radius-wall tension curves, the vessels were set up to a wall tension equal to two-thirds of the systolic blood pressure. In SHRs, the vessel diameters were reduced. After equilibration with Ringer's solution, vessel dilatation was decreased in calcium-free solution (10 +/- 3 vs. 34 +/- 7%, p less than 0.05), but contraction increased after 123 mM of potassium stimulation (78 +/- 19 vs. 33 +/- 9%). There was no difference in calcium sensitivity during methoxamine or potassium activation. In the coronary resistance vessels of SHRs, electron microscopy revealed media hypertrophy (15.6 +/- 2.9 vs. 9.5 +/- 2.1 microns, p less than 0.05) and media hyperplasia (4.5 +/- 3 vs. 3.7 +/- 6 muscle layers, p less than 0.05). Media hypertrophy and a decrease in the vasodilatating capacity of resistance vessels contribute to the reduction of coronary reserve in hypertensive hypertrophy. The minimal coronary vascular resistance, a parameter of the vasodilatating capacity, was significantly increased in SHRs. Antihypertensive therapy with metoprolol and hydralazine or nifedipine resulted in an improvement of coronary reserve.

Animals↗