Surgical Revascularization in Stable Ischemic Heart Disease
Surgical Revascularization in Stable Ischemic Heart Disease
A schema of this evolutionary process and the potential future is shown in Figure 6.
(Enlarge Image)
Figure 6.
The integrated status of intervention in stable ischemic heart disease. Highlights of the progression from anatomic-based intervention to physiologically augmented, quantified functional anatomic-based intervention over the past 50 years and into the future are depicted. This progression has fundamentally changed our understanding of R, and the benchmarks for deriving healthcare value from the R interventions.
CABG: Coronary artery bypass grafting; CAD: Coronary artery disease; CR: Complete revascularization; FFR: Fractional flow reserve; IR: Incomplete revascularization; OMT: Optimal medical therapy; PCI: Percutaneous coronary intervention; R: Revascularization; SIHD: Stable ischemic heart disease.
Two recent papers on SIHD help frame the future of surgical revascularization beyond the discussion thus far. The paper by Marzilli et al. proposes shifting ischemic heart disease emphasis away from obstructive epicardial coronary atherosclerosis, and centering it on the microvasculature and myocardial cell where the ischemia is taking place. They correctly point out that myocardial ischemia is a constellation of critical stenosis, inflammation, coagulopathy, spasm, endothelial dysfunction and microvascular dysfunction. Not all of these features will be present in all clinical events, but must be considered in all circumstances. Pepine and Douglas agree with the concept of a multifactorial model that includes vascular and cellular causes of ischemia, but argue against abandoning the potential link between epicardial atherosclerosis and ischemia. Rather, the problem inherent with obstruction as the etiology for ischemia is that obstruction does not always imply ischemia, and that ischemia does not always imply obstruction. Inherent in this debate is the continued elucidation of the extent to which physiology acts as the bridge between the epicardial coronary disease, the surrounding myocardium, these myocardial and cellular processes, and the impact that interventions might have on addressing this disharmonization of ischemia.
To achieve this, continued efforts by the Heart Team to understand the physiology of blood flow, perfusion and revascularization across the spectrum of SIHD will be needed. Pharmacologic improvements in OMT, new information in myocardial imaging of perfusion and ischemia, adoption of new technologies to better understand the physiology of revascularization in the catheterization laboratory, adoption of new technologies to better understand and quantify the physiology of revascularization in the operating room, and the opportunity to link these new physiologic data to short-, intermediate- and long-term outcomes will also be needed.
Since all patients require revascularization at a particular (but different) time point in SIHD, a clinical benefit must be accrued by: changing the underlying physiology by increasing blood flow and perfusion and/or altering the myocardial and cellular biology; slowing down the progression of the chronic disease; or both.
Since the disease process remains progressive, subsequent events are likely to occur (albeit at a reduced rate with OMT). The physiologic result of CABG must provide protection not necessarily against subsequent events occurring, but at a minimum against these events having clinical significance. Since both SYNTAX and FREEDOM interventions used anatomy for the intervention, the survival benefit must be influenced by something other than anatomy. A list of possible causes are presented in Box 2.
Kern has argued that there are physiologic sequelae in the coronary vasculature distal to where stents are placed in the proximal third of the epicardial coronary arteries; these observations fit nicely with Mazilli's nonanatomic construct for SIHD. With CABG, perhaps an excess of myocardial perfusion (perfusion reserve) created by multivessel revascularization could explain at a physiologic and functional level why subsequent clinical events might occur, but without the clinical significance they may otherwise have. The increase in myocardial perfusion seen in 80% or more of OPCAB patients in our imaging series suggests that this might be the case.
Also with CABG, the myocardial integrity issues including collateral perfusion may be critical to the mechanism for improved long-term survival, with the architecture for the perfusion reserve to move blood where it is needed, based on the underlying functionality in place at the time. The intraoperative imaging of collateral flow resulting from TVECA revascularization at OPCAB is evidence of the dynamic nature of the myocardial perfusion engineered by the heart.
Indeed, the nonanatomic and nonfunctional components that are suggested by Pepine and Douglas are largely microvascular, physiologic influences that impact regional myocardial perfusion, and the perfusion exchange between different regions of the myocardium are variably supplied by epicardial coronary arteries with functional and/or anatomic stenoses. Our preliminary analyses comparing anatomy versus functional anatomy on the change in regional myocardial perfusion regionally and globally document that functional anatomy, but not anatomy alone, correlates with the change in perfusion. This suggests that what is being imaged is the relief of ischemia or a perfusion deficit (measured by FFR). Since in humans, basal myocardial blood flow remains constant regardless of the severity of a coronary stenosis, these new data suggest that the characteristics of the ischemic myocardium are driving the measured change in perfusion, perhaps through a change in myocardial resistance with revascularization.
Sustainably altering myocardial perfusion is the physiologic outcome objective of modern ischemic heart disease intervention, because it is directly linked to improved long-term survival, as well as relief of symptoms. This objective will require attributes from all components of Figure 6; the common thread among all these components, however, is the physiology of blood flow and perfusion.
Next Steps
A schema of this evolutionary process and the potential future is shown in Figure 6.
(Enlarge Image)
Figure 6.
The integrated status of intervention in stable ischemic heart disease. Highlights of the progression from anatomic-based intervention to physiologically augmented, quantified functional anatomic-based intervention over the past 50 years and into the future are depicted. This progression has fundamentally changed our understanding of R, and the benchmarks for deriving healthcare value from the R interventions.
CABG: Coronary artery bypass grafting; CAD: Coronary artery disease; CR: Complete revascularization; FFR: Fractional flow reserve; IR: Incomplete revascularization; OMT: Optimal medical therapy; PCI: Percutaneous coronary intervention; R: Revascularization; SIHD: Stable ischemic heart disease.
Physiologically Defined, Quantified Functional Anatomy
Two recent papers on SIHD help frame the future of surgical revascularization beyond the discussion thus far. The paper by Marzilli et al. proposes shifting ischemic heart disease emphasis away from obstructive epicardial coronary atherosclerosis, and centering it on the microvasculature and myocardial cell where the ischemia is taking place. They correctly point out that myocardial ischemia is a constellation of critical stenosis, inflammation, coagulopathy, spasm, endothelial dysfunction and microvascular dysfunction. Not all of these features will be present in all clinical events, but must be considered in all circumstances. Pepine and Douglas agree with the concept of a multifactorial model that includes vascular and cellular causes of ischemia, but argue against abandoning the potential link between epicardial atherosclerosis and ischemia. Rather, the problem inherent with obstruction as the etiology for ischemia is that obstruction does not always imply ischemia, and that ischemia does not always imply obstruction. Inherent in this debate is the continued elucidation of the extent to which physiology acts as the bridge between the epicardial coronary disease, the surrounding myocardium, these myocardial and cellular processes, and the impact that interventions might have on addressing this disharmonization of ischemia.
To achieve this, continued efforts by the Heart Team to understand the physiology of blood flow, perfusion and revascularization across the spectrum of SIHD will be needed. Pharmacologic improvements in OMT, new information in myocardial imaging of perfusion and ischemia, adoption of new technologies to better understand the physiology of revascularization in the catheterization laboratory, adoption of new technologies to better understand and quantify the physiology of revascularization in the operating room, and the opportunity to link these new physiologic data to short-, intermediate- and long-term outcomes will also be needed.
Since all patients require revascularization at a particular (but different) time point in SIHD, a clinical benefit must be accrued by: changing the underlying physiology by increasing blood flow and perfusion and/or altering the myocardial and cellular biology; slowing down the progression of the chronic disease; or both.
Since the disease process remains progressive, subsequent events are likely to occur (albeit at a reduced rate with OMT). The physiologic result of CABG must provide protection not necessarily against subsequent events occurring, but at a minimum against these events having clinical significance. Since both SYNTAX and FREEDOM interventions used anatomy for the intervention, the survival benefit must be influenced by something other than anatomy. A list of possible causes are presented in Box 2.
Kern has argued that there are physiologic sequelae in the coronary vasculature distal to where stents are placed in the proximal third of the epicardial coronary arteries; these observations fit nicely with Mazilli's nonanatomic construct for SIHD. With CABG, perhaps an excess of myocardial perfusion (perfusion reserve) created by multivessel revascularization could explain at a physiologic and functional level why subsequent clinical events might occur, but without the clinical significance they may otherwise have. The increase in myocardial perfusion seen in 80% or more of OPCAB patients in our imaging series suggests that this might be the case.
Also with CABG, the myocardial integrity issues including collateral perfusion may be critical to the mechanism for improved long-term survival, with the architecture for the perfusion reserve to move blood where it is needed, based on the underlying functionality in place at the time. The intraoperative imaging of collateral flow resulting from TVECA revascularization at OPCAB is evidence of the dynamic nature of the myocardial perfusion engineered by the heart.
Indeed, the nonanatomic and nonfunctional components that are suggested by Pepine and Douglas are largely microvascular, physiologic influences that impact regional myocardial perfusion, and the perfusion exchange between different regions of the myocardium are variably supplied by epicardial coronary arteries with functional and/or anatomic stenoses. Our preliminary analyses comparing anatomy versus functional anatomy on the change in regional myocardial perfusion regionally and globally document that functional anatomy, but not anatomy alone, correlates with the change in perfusion. This suggests that what is being imaged is the relief of ischemia or a perfusion deficit (measured by FFR). Since in humans, basal myocardial blood flow remains constant regardless of the severity of a coronary stenosis, these new data suggest that the characteristics of the ischemic myocardium are driving the measured change in perfusion, perhaps through a change in myocardial resistance with revascularization.
Sustainably altering myocardial perfusion is the physiologic outcome objective of modern ischemic heart disease intervention, because it is directly linked to improved long-term survival, as well as relief of symptoms. This objective will require attributes from all components of Figure 6; the common thread among all these components, however, is the physiology of blood flow and perfusion.
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