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External Compression of Epicardial Coronary Arteries with Partial Calcific Pericarditis.

ABSTRACT: Calcific pericarditis (CP) is a rare disease which results from long-standing pericardial inflammation. Pericardial calcification may completely or partially encase the ventricles, resulting in impaired diastolic filling. We present a case of a 53-year-old male who was incidentally found to have annular CP resulting in external compression of a large territory diagonal branch (D1) reaching the apex with likely chronically occluded left anterior descending artery with collateral circulation from the right coronary artery with hemodynamic compromise on coronary angiography. This was emergently treated with a drug-eluting stent with improved D1 flow and entailed the importance of percutaneous coronary intervention as a viable option in cases of CP resulting in acute hemodynamic compromise.

SUBMITTER: Khan ZA

PROVIDER: S-EPMC5448248 | biostudies-literature | 2017 Jan-Mar

REPOSITORIES: biostudies-literature

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External Compression of Epicardial Coronary Arteries with Partial Calcific Pericarditis.

Khan Zubair Ahmed ZA Sardar Muhammad Rizwan MR Topalian Simon K SK

Heart views : the official journal of the Gulf Heart Association 20170101 1

Calcific pericarditis (CP) is a rare disease which results from long-standing pericardial inflammation. Pericardial calcification may completely or partially encase the ventricles, resulting in impaired diastolic filling. We present a case of a 53-year-old male who was incidentally found to have annular CP resulting in external compression of a large territory diagonal branch (D1) reaching the apex with likely chronically occluded left anterior descending artery with collateral circulation from ...[more]

PMID: 28584590

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Project description:1. Human epicardial coronary artery rings, freshly obtained from cardiac transplantation patients, commonly exhibited phasic contractile activity in vitro. This activity occurred either spontaneously or in response to vasoconstrictor stimulation. 2. Nifedipine pretreatment (1 nM-0.1 microM) reduced both types of phasic contractions in a concentration-dependent manner. At 0.1 microM nifedipine, spontaneous contractions were completely abolished, as were phasic contractions induced by U46619, endothelin-1 or 5-hydroxytryptamine (5-HT). 3. For U46619 (0.1-100 nM), the largest phasic contractions (amplitude peak to trough) occurred over the mid-range of concentrations used (1-10 nM). At higher concentrations (30-100 nM), phasic activity was reduced as the response reached a maximum. Estimated pEC50 values for the upper phasic and lower phasic curves were significantly different (8.71 +/- 0.13 versus 7.90 +/- 0.11; P < 0.05; n = 10). In the presence of nifidepine (0.1 microM), the purely tonic contraction curve to U46619 was similar to the lower phasic curve in the absence of nifedipine (pEC50 = 8.14 +/- 0.06, n = 10). Similar results were obtained for endothelin-1 (0.1-100 nM). 4. Responses to 5-HT (1 nM-3 microM) were more variable. The largest phasic contractions were spread unevenly throughout the concentration-response curve. In the presence of nifedipine (0.1 microM), the curve to 5-HT was significantly depressed in range but not sensitivity (pEC50) when compared with the phasic curves. 5. In conclusion, activation of dihydropyridine-sensitive voltage-operated Ca2+ channels mediated the phasic contractions commonly observed in human epicardial coronary arteries. These contractions amplified the contractile responses to low concentrations of vasoconstrictors. Inhibition of phasic activity by the Ca2+ channel antagonist, nifedipine, allowed the tonic vasoconstrictor profile of human isolated coronary artery to be determined which is important information for the accurate quantitative assessment of vasodilator responses in this tissue in vitro.

Project description:BACKGROUND:Enhanced External Counterpulsation (EECP) can chronically relieve ischemic chest pain and improve the prognosis of coronary heart disease (CHD). Despite its role in mitigating heart complications, EECP and the mechanisms behind its therapeutic nature, such as its effects on blood flow hemodynamics, are still not fully understood. This study aims to elucidate the effect of EECP on significant hemodynamic parameters in the coronary arterial tree. METHODS:A finite volume method was used in conjunction with the inlet pressure wave (surrogated by the measured aortic pressure) before and during EECP and outlet flow resistance, assuming the blood as newtonian fluid. The time-average wall shear stress (TAWSS) and oscillatory shear index (OSI) were determined from the flow field. RESULTS:Regardless of the degree of vascular stenosis, hemodynamic conditions and flow patterns could be improved during EECP. In comparison with the original tree, the tree with a severe stenosis (75% area stenosis) demonstrated more significant improvement in hemodynamic conditions and flow patterns during EECP, with surface area ratio of TAWSS risk area (SAR-TAWSS) reduced from 12.3% to 6.7% (vs. SAR-TAWSS reduced from 7.2% to 5.6% in the original tree) and surface area ratio of OSI risk area (SAR-OSI) reduced from 6.8% to 2.5% (vs. SAR-OSI of both 0% before and during EECP in the original tree because of mild stenosis). Moreover, it was also shown that small ratio of diastolic pressure (D) and systolic pressure (S) (D/S) could only improve the hemodynamic condition mildly. The SAR-TAWSS reduction ratio significantly increased as D/S became larger. CONCLUSIONS:A key finding of the study was that the improvement of hemodynamic conditions along the LMCA trees during EECP became more significant with the increase of D/S and the severity degree of stenoses at the bifurcation site. These findings have important implications on EECP as adjuvant therapy before or after percutaneous coronary intervention (PCI) in patients with diffuse atherosclerosis.

Dataset Information

External Compression of Epicardial Coronary Arteries with Partial Calcific Pericarditis.

Publications

External Compression of Epicardial Coronary Arteries with Partial Calcific Pericarditis.

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