Collaterals and the recovery of left ventricular function after recanalization of a chronic total coronary occlusion

Werner, Gerald S.; Surber, Ralf; Kuethe, Friedhelm; Emig, Ulf; Schwarz, Gero; Bahrmann, Philipp; Figulla, Hans R.

doi:10.1016/j.ahj.2004.04.042

Cited by 127 publications

(52 citation statements)

References 40 publications

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“…The possibility of LV functional recovery with its beneficial effect on survival provides the rationale for the technically demanding attempt to recanalize a CTO. 35 The recovery of impaired systolic LV function after revascularization of a CTO appears not to depend on the quality of collateral function, 36 suggesting that collateral development does not depend on the presence of viable myocardium. Simultaneous assessment of regional LV function with the use of transthoracic tissue Doppler imaging and invasive collateral function has shown a statistically relevant association between systolic as well as diastolic LV function and collateral function in patients with CAD (Table).…”

Section: The Coronary Occlusion Model: Natural Versus Artificialmentioning

confidence: 99%

Assessment of the Human Coronary Collateral Circulation

et al. 2010

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Section: The Coronary Occlusion Model: Natural Versus Artificialmentioning

confidence: 99%

Assessment of the Human Coronary Collateral Circulation

et al. 2010

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“…Left ventricular systolic function has been demonstrated to improve after CTO PCI in patients with baseline LV dysfunction, [34][35][36][37][38][39][40][41][42] while no change in ejection fraction can be expected when the baseline LV function is normal. 42 Left ventricular function improvement is dependent on the maintenance of CTO target vessel patency 37,38 and on the viability of the perfused myocardial territory, 39,40 …”

Section: Dysfunctionmentioning

confidence: 99%

“…42 Left ventricular function improvement is dependent on the maintenance of CTO target vessel patency 37,38 and on the viability of the perfused myocardial territory, 39,40 …”

Section: Dysfunctionmentioning

confidence: 99%

Percutaneous Treatment of Coronary Chronic Total Occlusions Part 1: Rationale and Outcomes

Galassi

Grantham

Kandzari

et al. 2014

Interventional Cardiology Review

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A chronic total occlusion (CTO) is defined as a completely occluded coronary artery with no antegrade flow (thrombolysis in myocardial infarction [TIMI] 0 flow) for at least three months.1 CTOs are present in 15-30 % of patients undergoing coronary angiography.2-5 In a Canadian prospective registry of 14,439 patients undergoing coronary angiography a CTO was present in 18.4 % of all patients with significant coronary artery disease (CAD).2 Approximately 1/3-1/2 6,7 of patients undergoing CTO percutaneous coronary intervention (PCI) have had a prior acute myocardial infarction (MI). This suggests acute onset of the occlusion, whereas in the remaining patients gradual development of CTO from high-grade lesions likely occurred.The basic histopathologic feature of a CTO is a proximal cap of the occlusion. This is often fibrotic or calcified and may provide considerable resistance to wire advancement during CTO PCI. Distal to the proximal cap and along the occlusion length follows a segment of loose fibrous tissue or organised thrombus, with various extent of calcification. 8,9 In several of these lesions, residual channels may be observed that are not visible under angiography. In addition, microchannels may appear during the CTO's consolidation process, however these are mostly located in the adventitia with extremely tortuous courses and do not generally traverse the entire occluded segment.10 A recent autopsy study of 95 CTO lesions from 82 patients reported frequent negative remodelling of the CTO body (more frequent with longer duration of the occlusion), very rare presence of microchannels and more frequent tapering of the distal cap as compared with the proximal cap (79 % vs. 50 %, P<0.0001). Successful CTO percutaneous coronary intervention (PCI) can significantly improve angina and improve left ventricular function. Although currently unproven, successful CTO PCI might also reduce the risk for arrhythmic events in patients with ischaemic cardiomyopathy, provide better tolerance of future acute coronary syndrome, and possibly improve survival. Evaluation by a heart team comprised of both interventional and non-interventional cardiologists and cardiac surgeons is important for determining the optimal revascularisation strategy in patients with coronary artery disease and CTOs. Ad hoc CTO PCI is generally not recommended, so as to allow sufficient time for (a) discussion with the patient about the indications, goals, risks, and alternatives to PCI; (b) careful procedural planning; and (c) contrast and radiation exposure minimisation. Use of drug-eluting stents is recommended for CTO PCI, given the lower rates of angiographic restenosis compared to bare metal stents.

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“…However, a substantial number of patients with CTO reveal various degrees of systolic LV dysfunction. The recovery of impaired systolic LV function after revascularization of a CTO seems not to depend on the quality of collateral function, 23 suggesting that collateral development does not depend on the presence of viable myocardium. In patients with CAD without CTO and viable myocardium, simultaneous assessment of regional LV function using transthoracic tissue Doppler imaging and invasive collateral function has shown an association between systolic as well as diastolic LV function and collateral function 24 (Table 2).…”

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Assessment and Impact of the Human Coronary Collateral Circulation on Myocardial Ischemia and Outcome

Seiler

2013

Circ: Cardiovascular Interventions

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Appropriate for risk stratification and clinical studies ACS indicates acute coronary syndrome; AP, angina pectoris; CFI p , pressure-derived collateral flow index; CFI v , velocity-derived collateral flow index; CPI, collateral perfusion index; CTO, chronic total (coronary) occlusion; and LV, left ventricle. threshold of 11 heartbeats accurately distinguishes between collateral supply sufficient or insufficient to prevent myocardial ischemia during a brief occlusion (sensitivity of 88%, specificity of 81% 28 ; Table 2). Quantitative Coronary Pressure and Doppler Sensor MeasurementsIn addition to their principle angiographic results, Rentrop et al 27 first described an angioplasty balloon occlusion model using the ratio between distal coronary occlusive or wedge pressure (P occl ) and aortic pressure (P ao ), which correlates with angiographic collateral score groups in patients with 1-vessel CAD (Table 2). 29 In 1987, Meier et al 30 found that a P occl ≥30 mm Hg accurately predicted the presence of spontaneously visible or recruitable collaterals. However, P occl is not dependent only on the amount of collateral flow to the occluded vascular region. Determinants of P occl are the driving pressure across collateral pathways (ie, the pressure difference between the coronary pressure in the collateral supplying and receiving artery), the venous back pressure (central venous or right atrial pressure), but also extravascular pressure related to compression of intramural vessels by cardiac contraction and to transmission of diastolic LV pressure to the epicardial circulation. 31 In this context, in that of microembolization of the collateral-dependent vascular area, P occl should not be used for collateral assessment in the acute coronary syndrome because collateral function is substantially overestimated. In the setting of chronic CAD, LV filling pressure has, however, no influence on P occl unless it exceeds values of 30 mm Hg.In 1993, Pijls et al 32 provided the experimental basis for the determination of maximum coronary and myocardial fractional blood flow by coronary pressure measurements; importantly, the contribution to myocardial blood flow by collateral pathways was assumed negligible. In this study, microvascular resistance during pharmacologically induced hyperemia was postulated to be constant and minimal and, thus, no longer dependent on the degree of epicardial stenoses. As a consequence, coronary pressure should directly reflect coronary flow, the former of which is more easily obtainable during invasive examination than the latter. Therefore, myocardial flow Q distal to a stenosis (the sum of flow through the stenotic vessel plus collateral flow as assumed to be zero) relative to myocardial flow without the stenosis Q N (Q/ Q N =fractional flow reserve, FFR) could be calculated on the basis of distal coronary pressure and aortic pressure both after subtraction of central venous backpressure (CVP). The model was tested in dogs, whereby Doppler-derived measurements of stenotic coronary flow Q s to norm...

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Collaterals and the recovery of left ventricular function after recanalization of a chronic total coronary occlusion

Cited by 127 publications

References 40 publications

Assessment of the Human Coronary Collateral Circulation

Assessment of the Human Coronary Collateral Circulation

Percutaneous Treatment of Coronary Chronic Total Occlusions Part 1: Rationale and Outcomes

Assessment and Impact of the Human Coronary Collateral Circulation on Myocardial Ischemia and Outcome

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