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Since the right and left ventricles (RV and LV) function under different loading conditions, it is not surprising that they differ in their mechanics (intramyocardial pressure), structure, and metabolism; such differences may also contribute to differences in the coronary vessel wall. Our hypothesis is that intima-media thickness (IMT), IMT-to-radius (IMT-to-R) ratio, and vessel wall stress vary transmurally in the LV, much more than in the RV. Five normal Yorkshire swine were used in this study. The major coronary arteries were cannulated through the aorta and perfusion fixed with 6.25% glutaraldehyde and casted with a catalyzed silicone-elastomer solution. Arterial and venous vessels were obtained from different transmural locations of the RV and LV, processed for histological analysis, and measured with an imaging software. A larger transmural gradient was found for IMT, IMT-to-R ratio, and diastolic circumferential stress in vessels from the LV than the nearly zero transmural slope in the RV. The IMT of arterial vessels in the LV showed a slope of 0.7 [+ or -] 0.5 compared with 0.3 [+ or -] 0.3 of arterial vessels in the RV (P [less than or equal to] 0.05). The slope for venous vessels in the LV was 0.14 [+ or -] 0.14 vs. 0.06 [+ or -] 0.05 in the RV. The present data reflect the local structure-function relation, where the significant gradient in intramyocardial pressure in the LV is associated with a significant gradient of IMT and IMT-to-R ratio, unlike the RV. This has important implications for local adaptation of transmural loading on the vessel wall and vascular remodeling when the loading is perturbed in cardiac hypertrophy or heart failure. coronary arteries; coronary veins; wall morphometry; wall stress; order number

The sudden exposure of veins to arterial pressures during coronary venous retroperfusion may cause rupture of small venules. Our rationale is to first occlude the coronary vein, which will cause an increase in pressure intermediate to arterial and venous values, and hence lead to remodeling and increased wall thickness of the veins prior to retroperfusion. To accomplish this objective, five pigs were subjected to left anterior descending (LAD) vein ligation while six pigs served as sham. Myocardial tissue samples were obtained from the area adjacent to the LAD vein at four transmural locations of the left ventricular free wall: epicardial surface, subepicardium, midmyocardium, and endocardium. Arterioles and venules from the experimental and sham control groups were photographed, and the following measurements were made: inner and outer circumferences, inner and outer areas, major and minor diameters, and intima-media thickness. Each vessel was categorized in tour different orders according to lumen diameter. Our results show that intima-media thickness was larger in the experimental group in all four regions of the heart and in all four orders of the vessels, although venules from the epicardial region showed the largest increase in thickness. The intima-media thickness-to-radius ratio was also larger in the experimental group and decreased from epicardial to endocardial region of the heart and from order 1 to order 4 of the vessels. The present study provides a rationale for the development of coronary retroperfusion strategy that avoids vessel rupture and hemorrhage in the postcapillary venules. pressure overload; arterialization; rupture stress; remodeling; ligation doi:10.1152/ajpheart.00235.2006

The pressure-induced remodeling of coronary veins is important in coronary venous retroperfusion. Our hypothesis is that the response of the large coronary veins to pressure overload will depend on the degree of myocardial support. Eleven normal Yorkshire swine from either sex, weighing 31-39 kg, were studied. Five pigs underwent ligation of the left anterior descending (LAD) vein, and six served as sham-operated controls. The ligation of the coronary vein caused an increase in pressure intermediate to arterial and venous values. After 2 wk of ligation, the animals were euthanized and the coronary vessels were perfusion-fixed with glutaraldehyde. The LAD vein was sectioned, and detailed morphometric measurements were made along its length from the point of ligation near the base down to the apex of the heart. The structural remodeling of the vein was circumferentially nonuniform because the vein is partially embedded in the myocardium; it was also axially nonuniform because it is tethered to the myocardium to different degrees along its axial length. The wall area was significantly larger in the experimental group, whereas luminal area in the proximal LAD vein was significantly smaller in the same group compared with sham-operated controls. The wall thickness-to-radius ratio was also significantly larger in the experimental group in proportion to the increase in pressure. The major conclusion of this study is that the response of the vein depends on the local wall stress, which is, in part, determined by the surrounding tissue. Furthermore, the geometric remodeling of the coronary vein restores the circumferential stress to the homeostatic value. arterialization; pressure-overload; retroperfusion; wall stress; surrounding tissue

Although hemodynamics changes occur in heart failure (HF) and generally influence vascular function, it is not clear whether various HF models will affect the conduit vessels differentially or whether local hemodynamic forces or systemic factors are more important determinants of vascular response in HF. Here, we studied the hemodynamic changes in tachycardia or volume-overload HF swine model (created by either high rate pacing or distal abdominal aortic-vena cava fistula, respectively) on carotid, femoral, and renal arteries function and molecular expression. The ejection fraction was reduced by 50% or 30% in tachycardia or volume-overload model in four weeks, respectively. The LV end diastolic volume was increased from 65±22 to 115±78 ml in tachycardia and 67±19 to 148±68 ml in volume-overload model. Flow reversal was observed in diastolic phase in carotid artery of both models and femoral artery in volume-overload model. The endothelial function was also significantly impaired in carotid and renal arteries of tachycardia and volume-overload animals. The endothelial dysfunction was observed in femoral artery of volume-overload animals but not tachycardia animals. The adrenergic receptor-dependent contractility decreased in carotid and femoral arteries of tachycardia animals. The protein expressions of NADPH oxidase subunits increased in the three arteries and both animal models while expression of MnSOD decreased in carotid artery of tachycardia and volume-overload model. In conclusion, different HF models lead to variable arterial hemodynamic changes but similar vascular and molecular expression changes that reflect the role of both local hemodynamics as well as systemic changes in HF. [ABSTRACT FROM AUTHOR]

There is no doubt that scaling relations exist between myocardial mass and morphometry of coronary vasculature. The purpose of this study is to quantify several morphological (diameter, length, and volume) and functional (flow) parameters of the coronary arterial tree in relation to myocardial mass. Eight normal porcine hearts of 117-244 g (mean of 177.5 ± 32.7) were used in this study. Various coronary subtrees of the left anterior descending, right coronary, and left circumflex arteries were perfused at pressure of 100 mmHg with different colors of a polymer (Microfil) to obtain rubber casts of arterial trees corresponding to different regions of myocardial mass. Volume, diameter, and cumulative length of coronary arteries were reconstructed from casts to analyze their relationship to the perfused myocardial mass. Volumetric flow was measured in relationship with perfused myocardial mass. Our results show that arterial volume is linearly related to regional myocardial mass, whereas the sum of coronary arterial branch lengths, vessel diameters, and volumetric flow show an -3/4, 3/8, and 3/4.power-law relationship, respectively, in relation to myocardial mass. These scaling laws suggest fundamental design principles underlying the structure-function relationship of the coronary arterial tree that may facilitate diagnosis and management of diffuse coronary artery disease. [ABSTRACT FROM AUTHOR]

The potential of the coronary veins for revascularization has been evaluated by many investigators for more than a century. The major hurdle has been the damage of veins during sudden exposure to arterial pressure. The solution to this problem has typically involved the use of intricate and complicated apparatus and devices, which has prevented routine clinical utility in the catheterization laboratory. This review examines this old concept from a new perspective and proposes a novel hypothesis to address previous shortcomings. We speculate on an approach that may serve to eliminate the edema and hemorrhage that result during venous retroperfusion as the pressure is suddenly increased to arterial values. We propose the rationale to increase the venous pressure to arterial values more gradually to allow prearterializations of the veins before full exposure of arterial pressure. Finally, we discuss various possible indications for this selective autoretroperfusion strategy to combat myocardial ischemia in cardiogenic shock patients, ST-elevation myocardial infarct patients, no-option patients, and beyond. [ABSTRACT FROM AUTHOR]

Purpose: To provide proof of concept for a diagnostic method to assess diffuse coronary artery disease (CAD) on the basis of coronary computed tomography (CT) angiography., Materials and Methods: The study was approved by the Cleveland Clinic Institutional Review Board, and all subjects gave informed consent. Morphometric data from the epicardial coronary artery tree, determined with CT angiography in 120 subjects (89 patients with metabolic syndrome and 31 age- and sex-matched control subjects) were analyzed on the basis of the scaling power law. Results obtained in patients with metabolic syndrome and control subjects were compared statistically., Results: The mean lumen cross-sectional area (ie, lumen cross-sectional area averaged over each vessel of an epicardial coronary artery tree) and sum of intravascular volume in patients with metabolic syndrome (0.039 cm(2) ± 0.015 [standard deviation] and 2.71 cm(3) ± 1.75, respectively) were significantly less than those in control subjects (0.054 cm(2)± 0.015 and 3.29 cm(3)± 1.77, respectively; P < .05). The length-volume power law showed coefficients of 27.0 cm(-4/3) ± 9.0 (R(2) = 0.91 ± 0.08) for patients with metabolic syndrome and 19.9 cm(-4/3) ± 4.3 (R(2) = 0.92 ± 0.07) for control subjects (P < .05). The probability frequency shows that more than 65% of patients with metabolic syndrome had a coefficient of 23 or more for the length-volume scaling power law, whereas approximately 90% of the control subjects had a coefficient of less than 23., Conclusion: The retrospective scaling analysis provides a quantitative rationale for diagnosis of diffuse CAD.

Glagov's positive remodelling in the early stages of coronary atherosclerosis often results in plaque rupture and acute events. Because positive remodelling is generally diffused along the epicardial coronary arterial tree, it is difficult to diagnose non-invasively. Hence, the objective of the study is to assess the use of scaling power law for the diagnosis of positive remodelling of coronary arteries based on computed tomography (CT) images. Epicardial coronary arterial trees were reconstructed from CT scans of six Ossabaw pigs fed on a high-fat, high-cholesterol, atherogenic diet for eight months as well as the same number of body-weight-matched farm pigs fed on a lean chow (101.9±16.1 versus 91.5±13.1 kg). The high-fat diet Ossabaw pig model showed diffuse positive remodelling of epicardial coronary arteries. Good fit of measured coronary data to the length-volume scaling power law ( where L(c) and V(c) are crown length and volume) were found for both the high-fat and control groups (R(2) = 0.95±0.04 and 0.99±0.01, respectively). The coefficient, K(LV), decreased significantly in the high-fat diet group when compared with the control (14.6±2.6 versus 40.9±5.6). The flow-length scaling power law, however, was nearly unaffected by the positive remodelling. The length-volume and flow-length scaling power laws were preserved in epicardial coronary arterial trees after positive remodelling. K(LV) < 18 in the length-volume scaling relation is a good index of positive remodelling of coronary arteries. These findings provide a clinical rationale for simple, accurate and non-invasive diagnosis of positive remodelling of coronary arteries, using conventional CT scans.

Myocardial fractional flow reserve (FFR), an important index of coronary stenosis, is measured by a pressure sensor guidewire. The determination of FFR, only based on the dimensions (lumen diameters and length) of stenosis and hyperaemic coronary flow with no other ad hoc parameters, is currently not possible. We propose an analytical model derived from conservation of energy, which considers various energy losses along the length of a stenosis, i.e. convective and diffusive energy losses as well as energy loss due to sudden constriction and expansion in lumen area. In vitro (constrictions were created in isolated arteries using symmetric and asymmetric tubes as well as an inflatable occluder cuff) and in vivo (constrictions were induced in coronary arteries of eight swine by an occluder cuff) experiments were used to validate the proposed analytical model. The proposed model agreed well with the experimental measurements. A least-squares fit showed a linear relation as (Δp or FFR)(experiment) = a(Δp or FFR)(theory) + b, where a and b were 1.08 and -1.15 mmHg (r(2) = 0.99) for in vitro Δp, 0.96 and 1.79 mmHg (r(2) = 0.75) for in vivo Δp, and 0.85 and 0.1 (r(2) = 0.7) for FFR. Flow pulsatility and stenosis shape (e.g. eccentricity, exit angle divergence, etc.) had a negligible effect on myocardial FFR, while the entrance effect in a coronary stenosis was found to contribute significantly to the pressure drop. We present a physics-based experimentally validated analytical model of coronary stenosis, which allows prediction of FFR based on stenosis dimensions and hyperaemic coronary flow with no empirical parameters.