Microvascular Dysfunction in Chronic Total Coronary Occlusions

Werner, Gerald S.; Ferrari, Markus; Richartz, Barbara M.; Gastmann, Oliver; Figulla, Hans R.

doi:10.1161/hc3401.095098

Cited by 41 publications

(29 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…14,16,18 The assumption that large collaterals, because of a low resistance, would not show steal 25 was confirmed by our study, because large collaterals were only observed in group R but not in group S. The lack of a vasodilatory reserve is demonstrated by the unchanged R P in group S, whereas it was decreased significantly in group R. On the other hand, the higher R P in group N and its lack of response to adenosine could be related to the higher proportion of diabetics with a known prevalence of microvascular dysfunction. 27 We did not record directly the coronary pressure in the donor artery at the collateral origin. The multiple coexisting collateral pathways make such an approach difficult and unreliable; in only 2 of 13 patients with steal we observed a singular collateral takeoff.…”

Section: Direct Confirmation Of the Collateral Network Model In Manmentioning

confidence: 99%

Direct Assessment of Coronary Steal and Associated Changes of Collateral Hemodynamics in Chronic Total Coronary Occlusions

Werner

Figulla

2002

Circulation

Self Cite

View full text Add to dashboard Cite

Background-Coronary steal can occur in collateral-dependent myocardium during pharmacologically induced vasodilation. This study assessed coronary steal invasively in chronic total coronary occlusions (TCOs). Methods and Results-In 35 consecutive patients with a percutaneous transluminal coronary angioplasty of a TCO (duration Ͼ4 weeks), coronary flow velocity (APV) by a Doppler wire and distal pressure (P D ) by a pressure wire were assessed in the collateral-dependent vascular bed before dilatation. Indexes of peripheral resistance (R P ) and for the collateral pathway, including the donor artery segment (R CP ), were calculated. Changes of these parameters were assessed during intravenous adenosine (140 g · kg Ϫ1 · min Ϫ1 ). Adenosine caused a decrease of APV, ie, coronary steal, in 13 patients (37%; group S), an increase in 11 patients (group R), and no change in 11 patients (group N). Angiographic analysis of collateral pathways showed no difference between the groups, except that in group S all collateral connections were continuously visible but no large collaterals (Ͼ0.5 mm) were found. In group N, collaterals were least developed. The increase of APV in group R was associated with a decrease of R P , whereas R CP remained unchanged. In contrast, group S showed no change in R P but a significant increase of R CP , indicating an increased resistance of the donor segment. Conclusions-Coronary

show abstract

Section: Direct Confirmation Of the Collateral Network Model In Manmentioning

confidence: 99%

Direct Assessment of Coronary Steal and Associated Changes of Collateral Hemodynamics in Chronic Total Coronary Occlusions

Werner

Figulla

2002

Circulation

Self Cite

View full text Add to dashboard Cite

show abstract

“…Opening a chronic totally occluded vessel with percutaneous angioplasty alters the microcirculatory responses (7,8). Abrupt occlusion of a newly recanalized chronic total coronary artery occlusion may result in an MI even though substantial preexisting collaterals protected the myocardium before opening the occlusion.…”

Section: See Page 15mentioning

confidence: 99%

Attenuated Coronary Collateral Function After Drug-Eluting Stent Implantation

Kern¹

2007

Journal of the American College of Cardiology

View full text Add to dashboard Cite

Caution has been, and should continue to be, the watchword for coronary artery stent implantation. Astute cardiologists should not be lulled to sleep in the face of the overwhelming everyday success of their expert interventional colleagues' skill in the use of drug-eluting stents (DES). Despite its revolutionary advances, DES implantation has a downside. In addition to the rare complications known to occur during the implantation procedure (extensive dissection, emboli, perforation, side branch occlusion, early abrupt closure, and so on), DES are associated with late subacute thrombosis despite perfect implantation technique and concomitant antiplatelet therapy (1). See page 15In this issue of the Journal, Meier et al.(2) identify a new downside to DES: the late attenuation of collateral function. Recall that the most important, if not the only, role of coronary collaterals is to protect the myocardium from ischemia. The rate and type of collateral recruitment with or without angiogenesis vary greatly and for reasons not completely understood (3). Acute recruitment of collateral flow can be demonstrated in some normal hearts without coronary artery disease (4). However, in most but not all patients with chronic ischemic heart disease, collaterals are recruited slowly, forming gradually over time. Responding to loss of distal coronary perfusion pressure and intermittent ischemia, angiogenic growth factors and other mediators are postulated to promote formation of new capillary pathways, thus improving perfusion to the challenged myocardial bed (5,6). In other patients, for example, some acute myocardial infarction (MI) patients, collaterals are acutely recruited, opening immediately during abrupt arterial occlusion and serving to limit what would otherwise be extensive MI.It is also important to note that collateral function can change after coronary intervention. Opening a chronic totally occluded vessel with percutaneous angioplasty alters the microcirculatory responses (7,8). Abrupt occlusion of a newly recanalized chronic total coronary artery occlusion may result in an MI even though substantial preexisting collaterals protected the myocardium before opening the occlusion. The restored perfusion after percutaneous coronary intervention (PCI) changed the collateral bed responses for the worse (9). Collateral function after stenting. Meier et al. (2) studied 120 patients undergoing repeat PCI 6 months after baremetal stent (BMS, n ϭ 60) and DES (n ϭ 60) implantation, matching patients for clinical and angiographic features including the in-stent stenosis severity. The collateral flow index (CFI ϭ coronary occlusion pressure/aortic pressure Ϫ central venous pressure) was measured during stent implantation using a pressure sensor angioplasty guidewire and invasively determined again at a follow-up catheterization. The functional impact of collaterals was also correlated to ischemic tolerance, as measured by intracoronary electrogram ST-segment elevation (Ն0.1 mV) during ischemia induced by balloon coronary occlu...

show abstract

“…In the time until the 3-mo follow-up, 30% of normal segments in the recanalized area developed a perfusion-metabolism mismatch in the group that had not been given progenitor cells. This deterioration could be attributable to disturbances in microvascular circulation or insufficient blood flow due to persistent paradoxical vasoconstriction of epicardial vessels (8). Because only patients with a successful recanalization (TIMI flow grade 3 with a residual stenosis of ,30%) were included in the study and no flow-limiting in-stent restenosis occurred (11), the deterioration in perfusion and development of a perfusionmetabolism mismatch in the placebo group was likely due FIGURE 2.…”

Section: Discussionmentioning

confidence: 99%

“…However, the underlying mechanisms are not fully understood (7). One speculation is that parts of the myocardium are insufficiently supplied because of persistent paradoxical vasoconstriction of epicardial vessels and microvascular dysfunction (8).…”

mentioning

confidence: 99%

Effect of Progenitor Cells on Myocardial Perfusion and Metabolism in Patients After Recanalization of a Chronically Occluded Coronary Artery

Kendziorra¹,

Barthel²,

Erbs³

et al. 2008

J Nucl Med

View full text Add to dashboard Cite

Even after recanalization of a chronic total coronary occlusion, functional recovery is incomplete and parts of the myocardium remain hypoperfused. In this randomized, placebo-controlled, and double-blinded study, we investigated relative changes in myocardial perfusion and glucose metabolism induced by intracoronary administration of blood-derived circulating progenitor cells (CPCs), compared with the natural course in a control group after recanalization of total coronary occlusion. Methods: After recanalization of total coronary occlusion, 26 patients were randomly assigned to the CPC treatment or placebo group. Regional myocardial perfusion and glucose metabolism were assessed by 99m Tc-tetrofosmin SPECT and 18 F-FDG PET at baseline (after recanalization of total coronary occlusion) and 3 mo after the administration of 69 6 14 · 10 6 CPCs or cell-free serum, respectively. Segments were classified as ''normal,'' ''perfusion-metabolism mismatch'' (dysfunctional segments with a 99m Tc-tetrofosmin-18 F-FDG mismatch), or ''scar.'' Results: In contrast to the placebo group, CPC administration resulted in a significant decrease in the number of segments with a perfusionmetabolism mismatch, from 3.0 6 0.5 to 1.7 6 0.6 segments (P , 0.05 vs. baseline). Of the normal segments at baseline, 2.7% in the CPC group and 30% in the placebo group revealed a perfusionmetabolism mismatch at follow-up after 3 mo (P , 0.05 vs. placebo). Conclusion: Intracoronary administration of CPCs significantly reduces the amount of myocardium with a perfusionmetabolism mismatch and prevents areas with normal perfusion and metabolism after recanalization of total coronary occlusion from becoming dysfunctional during the next 3 mo. These results show that PET and SPECT can be used to monitor the effect of progenitor cells on myocardial integrity. More important, they provide evidence supporting expansion of the use of progenitor cell treatment to chronic coronary artery disease. Pat ients with total occlusion of a main coronary artery are known to benefit significantly from recanalization with regard to major cardiac events (1), long-term survival (2), improvement of left ventricular function (3), and myocardial flow reserve (4). Nevertheless, functional recovery is incomplete, and parts of the myocardium remain with a perfusionmetabolism mismatch (5-7). However, the underlying mechanisms are not fully understood (7). One speculation is that parts of the myocardium are insufficiently supplied because of persistent paradoxical vasoconstriction of epicardial vessels and microvascular dysfunction (8).Lately, experimental and clinical studies using progenitor cells have shown functional recovery and improved myocardial perfusion in chronic myocardial ischemia (9,10). To investigate whether progenitor cells also demonstrate such a benefit after recanalization of total coronary occlusion, we conducted a randomized, placebo-controlled, and doubleblinded study with intracoronary administration of bloodderived circulating progenitor cells (CPCs) in pat...

show abstract

Microvascular Dysfunction in Chronic Total Coronary Occlusions

Cited by 41 publications

References 49 publications

Direct Assessment of Coronary Steal and Associated Changes of Collateral Hemodynamics in Chronic Total Coronary Occlusions

Direct Assessment of Coronary Steal and Associated Changes of Collateral Hemodynamics in Chronic Total Coronary Occlusions

Attenuated Coronary Collateral Function After Drug-Eluting Stent Implantation

Effect of Progenitor Cells on Myocardial Perfusion and Metabolism in Patients After Recanalization of a Chronically Occluded Coronary Artery

Contact Info

Product

Resources

About