Cath Lab Digest - November 2007 - (Page 37)

NOVEMBER REVIEW Preserving Left Ventricular Function during Percutaneous Coronary Intervention Prithwish Banerjee, MD and Dip Card, MRCP Department of Cardiology, University Hospitals Coventry & Warwickshire, United Kingdom Abstract The heart failure epidemic is predominantly an effect of widespread coronary disease, better treatment of coronary heart disease and an aging population. While coronary intervention prevents left ventricular systolic dysfunction (LVSD) by preventing or limiting myocardial damage, it can also be a cause of (iatrogenic) LVSD. Limiting myocardial damage during coronary intervention may well be the next important step that interventional cardiologists need to take by qualifying each procedure as high or low risk for the induction of LVSD and using an appropriate strategy that minimizes the risk of LVSD. This article discusses the various options of limiting LVSD during coronary intervention. Reprinted with permission from J INVASIVE CARDIOL 2007;19:440–443. P erhaps we interventionists should be more aware than we currently are of our patients’ left ventricular (LV) function or what angioplasty might do to that LV function. I am not suggesting that we don’t attach importance to this vital detail. But let’s face it, most of us don’t consciously plan to preserve myocardium at all costs when we are confronted with a difficult bifurcation lesion. To the battle-ravaged ventricle that has endured the torment of hypertension, diabetes, a few previous nonST-elevation myocardial infarctions (NSTEMIs), along with the regular pulses of alcohol thrown in, losing even a not-too-substantial side branch could well be the turning point on the mortality curve. Sometimes the situation demands that the sacrifice be made for “a greater good,” and that’s fair enough. However, let us remind ourselves that angioplasty, particularly elective percutaneous coronary intervention (PCI), is a cause of iatrogenic LV systolic dysfunction and may be more of a problem than we imagine or know (I am not aware of a randomized trial on this). Relationship between myocardial necrosis and LV systolic function. Myocardial necrosis following myocardial infarction (MI) leads to LV dilatation, followed by LV systolic dysfunction as a result of remodeling. Cardiac remodeling is generally accepted as a determinant of the clinical course of heart failure. Early infarct expansion occurs as the result of lengthening of the noncontractile region undergoing a stress response with secondary volume overload hypertrophy and is often progressive over time.1,2 About 26% of patients with acute myocardial infarction (AMI) develop limited dilatation and a further 20% progressive LV dilatation starting within hours-to-days after AMI, leading to significant LV systolic dysfunction at 1.5- and 3-year follow up.2 The process of ventricular enlargement can be influenced by three interdependent factors: infarct size, infarct healing and ventricular wall stresses.1 A useful way to prevent or minimize the increase in ventricular size after infarction and the consequent adverse effect on prognosis is to limit the initial insult. Acute reperfusion therapy has been consistently shown to result in a reduction in ventricular volume. The reestablishment of blood flow to the infarcted region, even beyond the time frame for myocyte salvage, has beneficial effects in limiting ventricular enlargement. Drug therapy with angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor-blockers (ARB), beta-blockers and aldosterone antagonists have all been shown to limit or reverse remodeling if started early in the post-infarct stage.3,4 Evidence of the effect of PCI on LV function at medium- and longterm follow up. Effect on LV systolic function. Bolognese et al 5 examined 284 consecutive patients undergoing primary percutaneous coronary intervention (PCI) for AMI by assessing LV function via echocardiographic and angiographic studies at 24 hours, 1 month and 6 months. Despite excellent infarctrelated artery patency rates at 6 months, 30% of patients showed LV dilatation with a > 20% increase in end-diastole volume at 6 months compared with 24 hours. LV dilatation at 6 months was associated with severe long-term LV systolic dysfunction and a poor prognosis, irrespective of the type of LV remodeling — early, late or progressive. Another study using 3-dimensional transthoracic echocardiography found remodeling to occur in onethird of patients at 12 months following primary PCI for ST-elevation MI (STEMI).6 Successful rescue PCI within 3–24 hours of the onset of chest pain has been associated with improved LV systolic function at a mean follow-up period of 22 months.7 In this study, baseline and repeat ventriculograms were used to assess LV systolic function. Other studies of primary PCI have also reported improved LV systolic function compared to thrombolysis.8 Some other studies have suggested benefit in patients with hibernating myocardium.9 Interestingly, late PCI on persistent total occlusions 3–28 days after MI did not reduce rates of death, reinfarction or heart failure (or LV ejection fraction) compared with optimal medical therapy in the large OAT 10 and TOSCA 2 11 studies. There appears to be no role for routine delayed PCI in improving LVEF in stable patients with an occluded infarct-related artery after MI. Effect on LV diastolic function. One of the causes of diastolic dysfunction is coronary artery disease.12 Acute coronary syndromes (ACS) may present with acute heart failure purely as a result of exacerbation of diastolic dysfunction (in the absence of any systolic dysfunction).13 PCI does improve diastolic function in such patients but patients with hypertension (the most common subset of patients with diastolic dysfunction) and AMI have a higher propensity to develop heart failure post-primary PCI than those without hypertension.14 Henein and colleagues15 reported improvement in both systolic and diastolic function after successful angioplasty in a small study, attributing the baseline LV dysfunction to the coronary lesions. Diastolic dysfunction in coronary disease becomes more pronounced with aging and produces significant morbidity, especially if atrial fibrillation or systolic dysfunction is superimposed.13 Difficulties faced by interventionists. Let us look at the common scenarios during intervention. A lot of the elective PCI patients will have undergone LV angiography, and in those with preserved LV systolic function, losing a small side branch might not matter too much (although the numbers might add up in multivessel PCI if we are not careful). A number of PCI centers have adopted the “coronary angiography? proceed to PCI if needed” approach though, and perhaps in that setting of rapid, in-the-lab decision-making under time pressure, the importance of the recorded LV function fades slightly and takes second priority in the wider scheme of things, particularly with respect to the ensuing PCI procedure. It might be that if we had all signed up to the “no compromise on LV function if possible” approach beforehand, and had more time to review the pictures and consider a plan in relaxed circumstances, we would have noticed the mild LV systolic impairment and referred the patient for coronary artery bypass grafting (CABG) instead, given the complexity of the PCI procedure, despite complete confidence that a reasonable angiographic final result would be achieved, but also mindful that significant compromise of LV function cannot be guaranteed. Adopt a policy of limiting LV necrosis during PCI? I work at a center where we treat outpatient transfers from surrounding smaller hospitals. I am in contact with the transferred patient for a few hours only, between their entry to our cardiology outpatient unit, to their departure back to the referring hospital if the PCI goes well. Often,

Table of Contents Feed for the Digital Edition of Cath Lab Digest - November 2007

Henry Ford Heart and Vascular Institute Treating Patients with Complex Vascular Disease with a Multi-Disciplinary Approach Improving Patient Compliance with Antiplatelet Medications Clinical Editor’s Corner Cath Lab Nurse/Tech Vascular Access and Closure Using the StarClose® Device The Clinical and Economic Impact of Measuring Fractional Flow Reserve FFR and Choosing an Optimal Revascularization Strategy Finally! The New Registered Cardiac Electrophysiology Specialist (RCES) Credential Use of a Mobile Lab to ‘Test the Waters’ at a Rural Hospital Remembering a Cardiac Cath Lab History ACVP• Membership Page What Do You Think? The Ten-Minute Interview with… Ernie Livingston, RN, BSN SICP* Chapter Updates Who’s in Charge? Working to Eliminate Bottlenecks: Florida Hospital’s Cardiac Cath Lab Achieves Greater Efficiency and Higher Satisfaction Preserving Left Ventricular Function during Percutaneous Coronary Intervention Ask the Clinical Instructor: A Q&A Column for Those New to the Cath Lab Making the Most of Your First Impression: Interviewing Tips and Techniques CEU Education Center Clinical & Industry News Meetings Calendar

Cath Lab Digest - November 2007

For optimal viewing of this digital publication, please enable JavaScript and then refresh the page. If you would like to try to load the digital publication without using Flash Player detection, please click here.