scholarly journals Chronic coronary artery occlusion: when does the benefit outweigh the risk?

2019 ◽  
pp. 116-123
Author(s):  
A. G. Badoyan ◽  
D. A. Khelimsky ◽  
A. A. Shermuk ◽  
O. V. Krestyaninov ◽  
A. S. Bobrova ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Coronary Artery ◽  
Coronary Occlusion ◽  
Interventional Cardiology ◽  
Coronary Artery Occlusion ◽  
Evidence Base ◽  
Artery Occlusion ◽  
Endovascular Recanalization ◽  
Chronic Coronary Occlusion

Today, the treatment of patients with chronic coronary occlusion is one of the most difficult problems in interventional cardiology. This is due not only to the technical difficulties of endovascular recanalization, but also to the difficulty in selecting patients for whom revascularization will be beneficial. Due to the low evidence base and the conflicting results of large clinical trials, these patients are rarely referred for endovascular recanalization. The purpose of this article is to review the literature and systematize relevant knowledge on the management of patients with chronic coronary occlusion.

Exercise training improves endothelium-mediated vasorelaxation after chronic coronary occlusion

1999 ◽  
Vol 87 (5) ◽  
pp. 1948-1956 ◽  
Author(s):  
Kawanza L. Griffin ◽  
M. Harold Laughlin ◽  
Janet L. Parker
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery ◽  
Nitric Oxide Synthase ◽  
Exercise Training ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Chronic Coronary Occlusion ◽  
Enhanced Production ◽  
Oxide Synthase

The present study evaluated combined effects of chronic coronary occlusion and exercise training on endothelial function. Gradual occlusion was produced by placement of an ameroid constrictor around the proximal left circumflex (LCX) coronary artery of female swine. Two months after placement of the ameroid, animals were restricted to their pens or exercise trained for 16 wk. Epicardial arteries (>500 μm ID) were isolated from the collateral-dependent LCX coronary artery distal to the occlusion and the nonoccluded left anterior descending (LAD) coronary artery. Bradykinin- and ADP-mediated relaxation of LCX and LAD coronary arteries was enhanced after exercise training. Inhibition of nitric oxide synthase with N G-nitro-l-arginine methyl ester decreased bradykinin- and ADP-mediated relaxation in LCX and LAD myocardial regions. Importantly, combined inhibition of effects of endothelium-derived hyperpolarizing factor with increased extracellular K+ (20–30 mM) and nitric oxide synthase completely abolished coronary LAD and LCX relaxation to bradykinin. Our data indicate that exercise training improves endothelium-mediated relaxation of arteries isolated after chronic coronary artery occlusion, likely as a result of enhanced production of nitric oxide and endothelium-derived hyperpolarizing factor.

scholarly journals The retrograde technique for recanalization of chronically occluded coronary arteries: Case series report

2020 ◽  
pp. 124-124
Author(s):  
Stefan Juricic ◽  
Milorad Tesic ◽  
Milan Dobric ◽  
Srdjan Aleksandric ◽  
Zlatko Mehmedbegovic ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Case Series ◽  
Interventional Cardiology ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Special Technique ◽  
Retrograde Approach ◽  
Total Occlusion ◽  
Antegrade Approach ◽  
Increased Risk

Background. Chronic total occlusion (CTO) of coronary artery still represents one of the most challenging lesion subset in field of interventional cardiology. Considering the complexity and increased risk posed by the retrograde approach, it is most often performed after a failed antegrade approach. Methods. We present a series of cases dedicated to the retrograde approach as a special technique for the treatment of chronic total coronary artery occlusion. All cases have some special characteristics that are today part of a dedicated portfolio in every cath lab. Results. In our series of cases all of three percutaneous coronary interventions (PCI) with retrograde approach finished with successful recanalization of CTO with different strategy and supported with rotational atherectomy (RA) or intravascular ultrasound (IVUS). Conclusion. In cases where there is the presence of interventional collaterals, as well as when the anterograde approach is very difficult, the retrograde approach can increase the success rate of procedures. The retrograde approach requires a long learning curve as well as very skilled and experienced operators who are able to perform the procedure independently.

Loss of regional ventricular postextrasystolic potentiation after coronary occlusion in dogs

1977 ◽  
Vol 233 (3) ◽  
pp. H392-H348
Author(s):  
B. Crozatier ◽  
D. Franklin ◽  
P. Theroux ◽  
H. Tomoike ◽  
S. Sasayama ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Coronary Occlusion ◽  
Myocardial Function ◽  
Premature Ventricular Contraction ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Ventricular Contraction ◽  
Regional Myocardial Function ◽  
Irreversible Damage ◽  
Postextrasystolic Potentiation

Postextrasystolic potentiation following coronary artery occlusion was studied serially using pairs of ultrasonic crystals to measure regional myocardial function in control, marginally ischemic, and ischemic segments of the left ventricle in dogs. Prior to coronary occlusion (CO), percent shortening in control (normal) segments increased by an average of 51.4 +/- 4.6% in the beat after a premature ventricular contraction (post-PVC beat), and this response changed little after coronary occlusion. During the 1st min after CO, in ischemic segments, systolic expansion developed but was replaced by active shortening in post-PVC beats; however, after 3 min of CO (average) and thereafter, there was no net positive shortening in post-PVC beats. In marginally ischemic segments early after CO, hypokinesia developed, but there was marked augmentation of percent shortening (208.6 +/- 32.6%) which persisted in post-PVC beats even after 2 h. It is concluded that loss of postextrasystolic potentiation occurs rapidly in ischemic regions after CO and is not indicative of irreversible damage; partially ischemic regions retain this mechanism for prolonged periods.

Antifibrillatory effects of α1-adrenoceptor blocking drugs in experimental coronary artery occlusion and reperfusion

1993 ◽  
Vol 71 (2) ◽  
pp. 103-111 ◽  
Author(s):  
B. G. Benfey
Keyword(s):  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Guinea Pig ◽  
Ventricular Arrhythmias ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Coronary Reperfusion ◽  
Isolated Hearts ◽  
Anesthetized Dogs

The myocardium of animals and man possesses α1-adrenoceptors in addition to β-adrenoceptors. Ischemia increases sympathetic tone, and ventricular arrhythmias can occur by β- and α1-adrenoceptor stimulation. I believe that α1-adrenoceptor blocking drugs have antifibrillatory effects and will review the data that support this condition. The effect of α1,-adrenoceptor blocking drugs on the incidence of ventricular fibrillation in acute coronary artery occlusion and (or) reperfusion has been determined in 24 studies in conscious and anesthetized dogs and rats, anesthetized cats and pigs, and rat and guinea-pig isolated hearts. The drugs reduced the incidence of fibrillation from 35 to 24% in coronary occlusion and from 61 to 29% in reperfusion.Key words: heart, coronary occlusion, coronary reperfusion, ventricular fibrillation, α1-adrenoceptor blocking drugs.

VENTRICULAR FIBRILLATION INDUCED BY CORONARY OCCLUSION DURING HYPOTHERMIA IN DOGS AND THE EFFECTS OF QUINIDINE, QUINACRINE, AND OXYTOCIN

1963 ◽  
Vol 41 (1) ◽  
pp. 511-517 ◽  
Author(s):  
D. R. Varma ◽  
K. I. Melville
Keyword(s):  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Left Coronary Artery ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Surface Cooling ◽  
Normal Body Temperature ◽  
Oesophageal Temperature ◽  
Consistent Method

In dogs under pentobarbitone anesthesia, acute occlusion of the anterior descending branch of the left coronary artery at normal body temperature induced ventricular fibrillation in 30% of the animals, while hypothermia by surface cooling led to fibrillation in 40% of the animals. On the other hand, temporary coronary occlusion with hypothermia at 23 °C oesophageal temperature invariably induced ventricular fibrillation (15 experiments) within an average of 5.4 minutes of occlusion. Prior injections of quinidine and quinacrine protected 40 and 70%, respectively, of the dogs against this type of ventricular fibrillation (10 experiments each). Oxytocin (1–2 i.u./kg) offered no protection (six experiments) nor did it reverse established fibrillation under these conditions. It is concluded that temporary coronary artery occlusion at 23 °C oesophageal temperature in dogs is an effective and consistent method of producing ventricular fibrillation. It is also postulated that reduction of the coronary blood supply to the heart might be a precipitating factor in hypothermic ventricular fibrillation in surgery.

Baroreflex inhibition during coronary occlusion is mediated by prostaglandins

1989 ◽  
Vol 257 (1) ◽  
pp. R216-R223 ◽  
Author(s):  
I. H. Zucker ◽  
M. J. Panzenbeck ◽  
J. F. Hackley ◽  
K. Haiderzad
Keyword(s):  
Coronary Artery ◽  
Arterial Pressure ◽  
Coronary Occlusion ◽  
Strong Support ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Coronary Ischemia ◽  
Renal Sympathetic

The present study was undertaken to determine whether the baroreflex control of renal sympathetic nerve activity (RSNA) was attenuated by an acute coronary artery occlusion and if so, what was the role played by cardiac prostaglandins in this attenuation. Arterial pressure was lowered with an infusion of sodium nitroprusside before and during a 5- to 10-min occlusion of the left circumflex coronary artery. The protocol was repeated 30 min after indomethacin (5 mg/kg) had been given. In addition, this study was carried out in a group of vagotomized dogs and in a group of thoracic-sympathectomized dogs. In intact dogs, coronary occlusion reduced the slope of the mean arterial pressure-RSNA relationship by 75% from -7.7 +/- 1.8% change in RSNA per millimeter Hg before indomethacin treatment. After indomethacin, there was no inhibition of the baroreflex slope during coronary occlusion. The reduction in the slope during coronary occlusion was abolished in dogs that were vagotomized but preserved in thoracic-sympathectomized dogs. In this latter group, indomethacin inhibited the attenuation of the slope during coronary occlusion. These data provide strong support for the notion that some cyclooxygenase product (most likely a prostaglandin) is released during coronary ischemia and stimulates or sensitizes cardiac vagal afferent endings, which, in turn, attenuate the baroreflex-mediated increase in RSNA during lowered arterial pressure.

Interregional Differences in the Systolic and Diastolic Response of Nonischemic Myocardium to Remote Coronary Occlusion 

1999 ◽  
Vol 91 (3) ◽  
pp. 815-815 ◽  
Author(s):  
Stephan C. U. Marsch ◽  
Hernan R. Muñoz ◽  
Serge Dalmas ◽  
Pierre Foëx
Keyword(s):  
Coronary Artery ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Posterior Wall ◽  
Anterior Wall ◽  
Artery Occlusion ◽  
Regional Function ◽  
Circumflex Coronary Artery ◽  
Twofold Increase ◽  
Left Circumflex Coronary Artery

Background Previous work showed a twofold increase in stiffness of nonischemic myocardium at the base during ischemia of the left anterior wall. Whether the diastolic response of nonischemic myocardium to remote ischemia depends on the localization of the ischemic or the nonischemic area is unknown. Methods In dogs with open chests, regional function in ischemic and nonischemic myocardium was assessed (sonomicrometry) before and 5 min after occlusion of the left anterior descending coronary artery (LAD; n = 7) or the left circumflex coronary artery (LCX; n = 7). Results In nonischemic myocardium at the base, left anterior descending and left circumflex coronary artery occlusion both resulted in a twofold increase in chamber stiffness, whereas contractility and peak lengthening rate remained unchanged. In nonischemic myocardium of the posterior wall, left anterior descending coronary artery occlusion resulted in a significant (P<0.05 vs. control, P<0.05 vs. base) increase (mean+/-SD) in chamber stiffness (25+/-6%), contractility (17+/-5%), and peak lengthening rate (28+/-6%). In nonischemic myocardium at the apex, left circumflex coronary artery occlusion resulted in a significant (P<0.05 vs. control, P<0.05 vs. base) increase in chamber stiffness (15+/-5%), contractility (16+/-4%), and peak lengthening rate (19+/-6%). Conclusions Stiffening of remote nonischemic myocardium occurs regardless of the localization of the ischemic and nonischemic area. The systolic and diastolic responses of nonischemic myocardium are not necessarily homogenous but may vary among different regions.

TxA2 inhibition and ischemia-induced loss of myocardial function and reactive hyperemia

1990 ◽  
Vol 258 (5) ◽  
pp. H1402-H1408 ◽  
Author(s):  
J. L. Mehta ◽  
W. W. Nichols ◽  
R. Schofield ◽  
W. H. Donnelly ◽  
V. K. Chandna
Keyword(s):  
Coronary Artery ◽  
Coronary Occlusion ◽  
Myocardial Function ◽  
Reactive Hyperemia ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Leukocyte Infiltration ◽  
Coronary Reperfusion ◽  
Reperfusion Arrhythmias ◽  
Premature Ventricular Contractions

To determine the contribution of thromboxane (Tx) A2 release in reperfusion injury, 17 dogs were subjected to total coronary occlusion for 1 h and reperfusion for 1 h. Eleven dogs were treated with saline, and six were treated with selective TxA2 synthetase inhibitor U63,557A (5 mg/kg iv) 30 min before coronary artery occlusion. In all saline-treated dogs, peak reactive hyperemia after 10-s total coronary artery occlusion was diminished (P less than 0.01) after reperfusion. Myocardial segmental shortening was also reduced (9.8 +/- 1.9 to -6.7 +/- 2.0%, P less than 0.01) in the reperfused region. Reperfusion was associated with 737 +/- 343 premature ventricular contractions (PVCs) per hour. Histology revealed extensive myocardial infiltration and capillary plugging by leukocytes in the reperfused region. Myeloperoxidase, an index of leukocyte infiltration, was also increased (P less than 0.02) in the reperfused region. In the U63,557A-treated animals, serum and plasma TxB2 levels were markedly (P less than 0.02) reduced. Decrease in myocardial shortening fraction was less in U63,557A- than in saline-treated animals (P less than 0.05). The frequency of reperfusion PVCs was also significantly reduced (10 +/- 5 PVCs/h, P less than 0.02 compared with saline-treated dogs). However, peak reactive hyperemia was reduced similar to that in saline-treated dogs. Myocardial infiltration and capillary plugging by leukocytes in the reperfused regions was also similar in the U63,557A- and saline-treated dogs. These results indicate that treatment with U63,557A decreases reperfusion arrhythmias and preserves myocardial function. However, coronary reperfusion-induced deterioration in reactive hyperemia is not affected.(ABSTRACT TRUNCATED AT 250 WORDS)

VENTRICULAR FIBRILLATION INDUCED BY CORONARY OCCLUSION DURING HYPOTHERMIA IN DOGS AND THE EFFECTS OF QUINIDINE, QUINACRINE, AND OXYTOCIN

1963 ◽  
Vol 41 (2) ◽  
pp. 511-517 ◽  
Author(s):  
D. R. Varma ◽  
K. I. Melville
Keyword(s):  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Left Coronary Artery ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Surface Cooling ◽  
Normal Body Temperature ◽  
Oesophageal Temperature ◽  
Consistent Method

In dogs under pentobarbitone anesthesia, acute occlusion of the anterior descending branch of the left coronary artery at normal body temperature induced ventricular fibrillation in 30% of the animals, while hypothermia by surface cooling led to fibrillation in 40% of the animals. On the other hand, temporary coronary occlusion with hypothermia at 23 °C oesophageal temperature invariably induced ventricular fibrillation (15 experiments) within an average of 5.4 minutes of occlusion. Prior injections of quinidine and quinacrine protected 40 and 70%, respectively, of the dogs against this type of ventricular fibrillation (10 experiments each). Oxytocin (1–2 i.u./kg) offered no protection (six experiments) nor did it reverse established fibrillation under these conditions. It is concluded that temporary coronary artery occlusion at 23 °C oesophageal temperature in dogs is an effective and consistent method of producing ventricular fibrillation. It is also postulated that reduction of the coronary blood supply to the heart might be a precipitating factor in hypothermic ventricular fibrillation in surgery.

Regional myocardial blood flow and necrosis in primates following coronary occlusion

1984 ◽  
Vol 246 (4) ◽  
pp. H635-H639 ◽  
Author(s):  
M. Lavallee ◽  
S. F. Vatner
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Myocardial Blood Flow ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Border Zone ◽  
Regional Myocardial Blood Flow ◽  
Lateral Border ◽  
Regional Myocardial Blood

The effects of acute coronary artery occlusion on regional myocardial blood flow distribution in the remote nonischemic zone, the central ischemic zone, and the lateral border zone of the infarct were evaluated in conscious primates. Prior to coronary artery occlusion, blood flow was 1.51 +/- 0.11 in endocardial (Endo) and 1.36 +/- 0.11 ml X min-1g-1 in epicardial (Epi) layers with an Endo-to-Epi ratio of 1.17 +/- 0.05. Regional blood flow in the remote nonischemic zone increased by 28.0 +/- 4.7 and 31.7 +/- 3.6% for Endo and Epi layers, respectively, following coronary occlusion and remained elevated during the subsequent 24 h. At the center of infarct, Endo and Epi blood flows were depressed by 97.9 +/- 0.7 and by 97.9 +/- 0.8%, respectively, at 5 min after coronary occlusion and remained severely depressed throughout the 24-h observation period. Blood flow at the ischemic lateral border of the infarct was severely depressed and similar to the flow at the center of the infarct, whereas the nonischemic lateral border of the infarct had blood flow levels similar to the remote, nonischemic myocardium. Microsphere loss was not a feature of the primate infarct.

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