Pressure coronary

Space and time integration of the coronary perfusion flow yields the total blood flow to the LV. A classical experiment relating the total blood flow to the coronary pressure is simulated in Figure 9. The calculated classical autoregulating range are shown for two metabolic demands. The curvilinearity of the coronary flow pressure relationship, above and below this range, is due to the modification of the resistance by the increase of the coronary transmural pressures. 

Figure 9. Total coronary flow versus coronary pressure at different flow demands (Fd) calculated from Beyar and Sideman s (1984c) model.

Herep is the local coronary pressure andPq is a reference pressure (/ q = 13.3 kPa = 100 mmHg), jc is the distance in cm from the left ostium, and c is the wave speed in m s K The mean standard deviation of this correlation was 21 percent. 

Herep is local aortic pressure, is the previously noted reference pressure, andx is the distance from the aortic valve in cm. As may be seen, the pressure dependence derived here for the coronary arteries of the horse is on the order of twice that in Eq. (11) for the aorta of the dog. This is felt to reflect the less compliant character of the coronary vessels. It would have been desirable to obtain data such as presented in Rumberger et al. (1979) over a larger range in pressure. However, the pressure is determined by the carrier wave, i.e., the coronary pressure waveform, and although the range is limited, it is that of physiological interest. 

Figure 7. Coronary flow distribution versus coronary pressure.

Bellamy RF, Lowersohn JS (1980b) Effect of systole on coronary pressure flow relations in the right ventricles of the dog. Am J Physiol (Heart Circ Physiol 7) 238.H481-H486 Berne RM (1959) Cardiodynamics and the coronary circulation in hypothermia. An NY Acad Sci 80 365-383... 

Hanekamp, C. E., Koolen, J. J., Pijls, N. H., et al. (1999) Comparison of quantitative coronary angiography, intravascular ultrasound and coronary pressure measurement to assess optimum stent deployment. Circulation, 99, 1015-21. 

Hypertension is one of the two principal risk factors of many cardiovascular diseases, such as coronary heart disease (CHD), stroke, and CHF. Individuals are considered hypertensive if their systoHc arterial blood pressure is over 140 mm Hg (18.7 Pa) or their diastoHc arterial blood pressure is over 90 mm Hg (12 Pa). Over 60 million people, or one-third of the adult population in the United States are estimated to be hypertensive (163). About 90% of these patients are classified as primary or essential hypertensive because the etiology of their hypertension is unknown. It is generally agreed that there is a very strong genetic or hereditary component to this disease. 

Nicorandil. Nicorandil is a potassium channel opener that can lower blood pressure 21, 20, and 29 mm Hg after single oral doses of 10, 20, and 30 mg, respectively (250). There are no significant changes ia heart rate. Headache is the primary side effect. Nicorandil has potent coronary vasodilator effects. It causes sustained vasodilation of arteriolar resistance and venous capacitance blood vessels, thus reduciag cardiac preload and aftedoad. 

A third study (85) enrolled 7825 hypertensive patients (55% males and 45% females) having diastoHc blood pressures (DBP) of 99—104 mm Hg (13—14 Pa) there were no placebo controls. Forty-six percent of the patients were assigned to SC antihypertensive dmg therapy, ie, step 1, chlorthaUdone step 2, reserpine [50-55-5] or methyldopa [555-30-6], and step 3, hydralazine [86-54-4]. Fifty-four percent of the patients were assigned to the usual care (UC) sources in the community. Significant reductions in DBP and in cardiovascular and noncardiovascular deaths were noted in both groups. In the SC group, deaths from ischemic heart disease increased 9%, and deaths from coronary heart disease (CHD) and acute myocardial infarctions were reduced 20 and 46%, respectively. 

DHPs are potent arterial vasodilators. They act on resistance vessels and therefore reduce peripheral vascular resistance, lower arterial blood pressure, and antagonize vasospasms in coronary or peripheral arteries. By reducing afterload, DHPs also reduce cardiac oxygen demand. Together with their vascular spasmolytic effect, this explains most of the beneficial actions of DHPs in angina pectoris. Most DHPs are only licensed for the therapy of hypertension, some of them also for the treatment of angina pectoris and vasospastic (Prinzmetal) angina. 

In a third study the time course of the effects of intravenous and intracoronary injections of cysteinyl leukotrienes on metabolic parameters and systemic and coronary hemodynamics was examined in patients with normal coronary arteries [32]. LTD4 (3 nmol, injected into the left coronary artery) induced an early (20 s), transient fall in mean arterial pressure paralleled by rises in heart rate and plasma levels of epinephrine and norepinephrine, all of which had returned to baseline by 10 min. CVR rose at 10 and 15 min and myocardial oxygen extraction at 15 min. Thus, small doses of cysteinyl leukotrienes may induce both an early, transient fall in mean arterial pressure, with secondary sympathoadrenergic activation, and a later increase in small coronary arteriolar resistance. 

Cysteinyl leukotrienes can induce an early, transient fall in arterial pressure associated with sympathoadrenergic activation, plus a late rise in small coronary arteriolar resistance [32]. Using specific antagonists of CysFTi and CysFT2 [63] it will be possible to assess the each receptor s contribution to the cardiovascular effects of these vasoactive mediators. 

Additional factors considered to play a part in coronary heart disease include high blood pressure, smoking, male gender, obesity (particularly abdominal obesity), lack of exercise, and drinking soft as opposed to hard water. Factors associated with elevation of plasma FFA followed by increased output of triacylglycerol and cho-... 

Modern representations of the virtual heart, therefore, describe structural aspects like fibre orientation in cardiac muscle, together with the distribution of various cell types, active and passive electrical and mechanical properties, as well as the coupling between cells. This then allows accurate reproduction of the spread of the electrical wave, subsequent contraction of the heart, and effects on blood pressure, coronary perfusion, etc. It is important to point out, here, that all these parameters are closely interrelated, and changes in any one of them influence the behaviour of all others. This makes for an exceedingly complex system. 

The same applies to pathologically-disturbed function. A simulated reduction in coronary blood flow (heart attack) would lead to reduced oxygen supply to the cells in the virtual heart, which would reduce efficiency of cardiac contraction and possibly give rise to heart rhythm disturbances. Ventricular pressure development would be compromised, as would the blood supply to all organs of the body, including the heart. All these implications can be studied in a virtual heart. 

The individual modules of the in situ heart can be coupled together to compute a whole sequence from ventricular pressure development, coronary perfusion, tissue supply of metabolites, cell energy consumption, and electrophysiology, to contractile activity and ventricular pressure development in the subsequent beat. The starting point (here chosen as ventricular pressure development) can be freely selected, and drug effects on the system can be simulated. Inserted into a virtual torso, these models allow one to compute the spread of excitation, its cellular basis, and the consequences for an ECG under normal and pathological conditions. 

Increased oxygen demand secondary to increased heart rates and blood pressure has been hypothesized to lead to myocardial infarction (especially in patients with fixed coronary disease) and/or ventricular arrhythmias. In patients with no history of cardiac disease, cocaine is thought to induce acute isehemie complications via vasospasm of the coronaries (Ascher et al. 1988). In addition, Virmani et al. (1988) have reported a 20 percent incidence of myocarditis thought to be secondary to accumulated microvascular injuries. 

P-blocker therapy was ineffective in preventing coronary heart disease, cardiovascular mortality, and all-cause mortality when compared to diuretics for elderly patients (60 years of age or greater) treated for primary hypertension. Clearly, the effects of P-blockers on blood pressure are complex and difficult to ascribe to one or two mechanisms. Rather, the varied effects of negative chronotropic and inotropic properties along with reduced renin levels (Fig. 2-3) appear to result in an overall reduction in cardiac output and/or reduction in peripheral resistance. 

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