Anomalies of coronary arteries: do we know everything about them ?

2019 ◽  
Vol 22 (6) ◽  
pp. 10-12
Author(s):  
V. E. Sinitsyn

The editorial discusses the original article of E.F. Abbasov et al. “Epidemiology anomalies of coronary artery origin and course”. Editorial stresses high incidence of congenital coronary anomalies. It discusses types of such anomalies, their classifications and clinical significance. Myocardial “bridges” are the most frequent anomaly of coronary artery course. This anomaly is benign but in rare cases when obstruction of the coronary blood flow through the tunneled segment of the artery is suspected, use of additional functional tests (studies of myocardial perfusion or coronary blood flow) is recommended. It is important to note that coronary CT-angiography has advantages over traditional catheter angiography in detection of coronary anomalies.

Author(s):  
Soroush Nobari ◽  
Rosaire Mongrain ◽  
Richard Leask ◽  
Raymond Cartier

Coronary artery disease (CAD) is considered to be a major cause of mortality and morbidity in the developing world. It has recently been shown that aortic root pathologies such as aortic stiffening and calcific aortic stenosis can contribute to the initiation and progression of this disease by affecting coronary blood flow [1,2]. Such pathologies influence the distensibility of the aortic root and therefore the hemodynamics of the entire region. As a consequence the coronary blood flow and velocity profiles will be altered [3,4,5] which could accelerate the development of an existing coronary artery disease. However, it would be very interesting to see if an occluded coronary artery would have a mutual impact on valvular dynamics and aortic root pathologies. This bi-directionality could aggravate and contribute to the progression of both the coronary and aortic root pathology.


Author(s):  
Valentina Magagnin ◽  
Maurizio Turiel ◽  
Sergio Cerutti ◽  
Luigi Delfino ◽  
Enrico Caiani

The coronary flow reserve (CFR) represents an important functional parameter to assess epicardial coronary stenosis and to evaluate the integrity of coronary microcirculation (Kern, 2000; Sadamatsu, Tashiro, Maehira, & Yamamoto, 2000). CFR can be measured, during adenosine or dipyridamole infusion, as the ratio of maximal (pharmacologically stimulated) to baseline (resting) diastolic coronary blood flow peak. Even in absence of stenosis in epicardial coronary artery, the CFR may be decreased when coronary microvascular circulation is compromised by arterial hypertension with or without left ventricular hypertrophy, diabetes mellitus, hypercholesterolemia, syndrome X, hypertrophic cardiomyopathy, and connective tissue diseases (Dimitrow, 2003; Strauer, Motz, Vogt, & Schwartzkopff, 1997). Several methods have been established for measuring CFR: invasive (intracoronary Doppler flow wire) (Caiati, Montaldo, Zedda, Bina, & Iliceto, 1999b; Lethen, Tries, Brechtken, Kersting, & Lambertz, 2003a; Lethen, Tries, Kersting, & Lambertz, 2003b), semi-invasive and scarcely feasible (transesophageal Doppler echocardiography) (Hirabayashi, Morita, Mizushige, Yamada, Ohmori, & Tanimoto, 1991; Iliceto, Marangelli, Memmola, & Rizzon, 1991; Lethen, Tries, Michel, & Lambertz, 2002; Redberg, Sobol, Chou, Malloy, Kumar, & Botvinick, 1995), or extremely expensive and scarcely available methods (PET, SPECT, MRI) (Caiati, Cioglia, Montaldo, Zedda, Rubini, & Pirisi, 1999a; Daimon, Watanabe, Yamagishi, Muro, Akioka, & Hirata, 2001; Koskenvuo, Saraste, Niemi, Knuuti, Sakuma, & Toikka, 2003; Laubenbacher, Rothley, Sitomer, Beanlands, Sawada, & Sutor, 1993; Picano, Parodi, Lattanzi, Sambuceti, Andrade, & Marzullo, 1994; Saraste, Koskenvuo, Knuuti, Toikka, Laine, & Niemi, 2001; Williams, Mullani, Jansen, & Anderson, 1994), thus their clinical use is limited (Dimitrow, 2003). In addition, PET and intracoronary Doppler flow wire involve radiation exposure, with inherent risk, environmental impact, and biohazard connected with use of ionizing testing (Picano, 2003a). In the last decade, the development of new ultrasound equipments and probes has made possible the noninvasive evaluation of coronary blood velocity by Doppler echocardiography, using a transthoracic approach. In this way, the peak diastolic coronary flow velocity reserve (CFVR) can be estimated as the ratio of the maximal (pharmacologically stimulated) to baseline (resting) diastolic coronary blood flow velocity peak measured from the Doppler tracings. Several studies have shown that peak diastolic CFVR, computed in the distal portion of the left anterior descending (LAD) coronary artery, correlates with CFR obtained by more invasive techniques. This provided a reliable and non invasive tool for the diagnosis of LAD coronary artery disease (Caiati et al., 1999b; Caiati, Montaldo, Zedda, Montisci, Ruscazio, & Lai, 1999c; Hozumi, Yoshida, Akasaka, Asami, Ogata, & Takagi, 1998; Koskenvuo et al., 2003; Saraste et al., 2001).


1996 ◽  
Vol 26 (5) ◽  
pp. 968
Author(s):  
Seung-Jea Tahk ◽  
Won Kim ◽  
Jing-Song Shen ◽  
Joon-Han Shin ◽  
Han-Soo Kim ◽  
...  

1989 ◽  
Vol 257 (6) ◽  
pp. H1983-H1993 ◽  
Author(s):  
J. M. Capasso ◽  
M. W. Jeanty ◽  
T. Palackal ◽  
G. Olivetti ◽  
P. Anversa

To determine the consequence of acute nonocclusive constriction of the epicardial coronary artery on the adaptation of the left ventricle and its impact as a function of age, the left main coronary artery was narrowed in rats 4 and 12 mo of age, and the animals were killed 45 min later. Similar reductions in the luminal diameter, averaging 4%, were obtained in both groups of animals, and this change resulted in an increase in left ventricular end-diastolic pressure and a decrease in positive and negative change in pressure overtime (dP/dt) and in peak-developed ventricular pressure. Left ventricular volume increased by 66% and 56% at 4 and 12 mo because of increases in both the longitudinal and transverse chamber diameters. In contrast, wall thickness decreased by 27% and 35%, whereas sarcomere length increased only by 8.0% and 6.0%, respectively. These changes implied the occurrence of side-to-side slippage of myocytes within the wall to accommodate the larger chamber volume. The alterations in myocardial performance combined with the variations in ventricular size and wall thickness produced a marked elevation in diastolic and systolic wall stress. Moreover, myocyte cell damage in the form of contraction bands and disorganization of the intercalated disc region was seen. No consistent difference was found in any of the parameters measured as a function of age. Measurements of resting coronary blood flow across the left ventricular wall before coronary artery narrowing were comparable with those obtained 45 min after constriction. In conclusion, acute nonocclusive coronary artery stenosis has profound detrimental effects on the function and structure of the myocardium in the absence of an impairment of resting coronary blood flow.


2003 ◽  
Vol 95 (1) ◽  
pp. 81-88 ◽  
Author(s):  
Antonio Rodríguez-Sinovas ◽  
Josep Bis ◽  
Inocencio Anivarro ◽  
Javier de la Torre ◽  
Antoni Bayés-Genís ◽  
...  

This study tested whether ischemia-reperfusion alters coronary smooth muscle reactivity to vasoconstrictor stimuli such as those elicited by an adventitial stimulation with methacholine. In vitro studies were performed to assess the reactivity of endothelium-denuded infarct-related coronary arteries to methacholine ( n = 18). In addition, the vasoconstrictor effects of adventitial application of methacholine to left anterior descending (LAD) coronary artery was assessed in vivo in pigs submitted to 2 h of LAD occlusion followed by reperfusion ( n = 12), LAD deendothelization ( n = 11), or a sham operation ( n = 6). Endothelial-dependent vasodilator capacity of infarct-related LAD was assessed by intracoronary injection of bradykinin ( n = 13). In vitro, smooth muscle reactivity to methacholine was unaffected by ischemia-reperfusion. In vivo, baseline methacholine administration induced a transient and reversible drop in coronary blood flow (9.6 ± 4.6 to 1.9 ± 2.6 ml/min, P < 0.01), accompanied by severe left ventricular dysfunction. After ischemia-reperfusion, methacholine induced a prolonged and severe coronary blood flow drop (9.7 ± 7.0 to 3.4 ± 3.9 ml/min), with a significant delay in recovery ( P < 0.001). Endothelial denudation mimics in part the effects of methacholine after ischemia-reperfusion, and intracoronary bradykinin confirmed the existence of endothelial dysfunction. Infarct-related epicardial coronary artery shows a delayed recovery after vasoconstrictor stimuli, because of appropriate smooth muscle reactivity and impairment of endothelial-dependent vasodilator capacity.


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