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PubMed2002

The need for standardisation of cardiac FDG PET imaging in the evaluation of myocardial viability in patients with chronic ischaemic left ventricular dysfunction.

The evaluation of myocardial glucose utilisation with fluorine-18 fluorodeoxyglucose (FDG) and positron emission tomography is currently considered the most reliable tool for the identification of myocardial viability. However, the investigations using FDG imaging to predict improvement in left ventricular (LV) function after revascularisation have reported wide ranges for sensitivity (71%-100%) and, in particular, for specificity (33%-91%). The variable results may be related to differences in study populations but also to differences in the imaging protocols employed. Detailed analysis of the published studies has revealed differences in study populations, patient selection criteria, the methods for assessing changes in LV function post revascularisation and the timing of these assessments. Even more importantly, protocols have varied substantially with regard to imaging equipment, perfusion tracers, metabolic conditions, data analysis and interpretation of results. In addition, evaluation of patients with insulin resistance appears to represent a specific challenge. This review examines the different study protocols and methodologies used for myocardial FDG imaging in order to draw conclusions concerning optimal imaging protocols. It appears that the optimisation and standardisation of study protocols and analysis of FDG images for the assessment of myocardial viability are critical. In addition, multi-centre trials seem warranted on prediction of long-term function, congestive heart failure symptoms, survival and quality of life.

Fluorodeoxyglucose F18↗
PubMedDate not supplied

[Reversible left ventricular dysfunction in coronary disease (part one): myocardial stunning].

INTRODUCTION: The concept of myocardial stunning has been proposed by Braunwald and Kloner in early 1980's and is defined as transient postischemic myocardial dysfunction that persists after reperfusion, despite the absence of irreversible damage and restoration of normal or near normal coronary flow. Thus, the hallmark of stunned myocardium is the mismatch between coronary flow and myocardial function. MYOCARDIAL STUNNING: The two most plausible hypotheses used to explain the pathogenetic mechanisms of myocardial stunning are calcium and oxyradical hypotheses. According to the first one, myocardial stunning is the result of impaired calcium homeostasis caused either by calcium overload or decreased responsiveness of myofilaments to calcium. The oxyradical hypothesis postulates that generation of free oxygen radicals depresses myocardial function after the ischemic episode. The exact mechanism is unknown, but it is probably due to extreme reactivity of oxyradicals that bind to some cellular components, impairing membrane permeability and function of various cell organelle. Stunned myocardium can be seen in numerous clinical situations in which myocardial ischemia has been followed by reperfusion. These include: coronary artery bypass surgery, acute myocardial infarction, stable, unstable and variant angina, percutaneous transluminal coronary angioplasty and cardiac transplantation. DISCUSSION AND CONCLUSION: In majority of these situations, stunned myocardium is usually well tolerated. However, there is a group of high-risk patients in whom prolonged myocardial dysfunction due to stunning can cause serious hemodynamic instability, which requires pharmacological and/or mechanical support. Therefore, in order to avoid these situations, some authors have suggested that stunned myocardium should be prevented, rather than treated. Since stunned myocardium is by definition reperfused, with normal or near normal coronary flow, treatment is reserved only for those patients in whom stunned region is large enough to cause low cardiac output and hypotension. Revascularisation is usually unnecessary; however, there are situations in which episodes of repetitive stunning cause chronic myocardial dysfunction along with hibernated myocardium, when myocardial revascularization would be beneficial.

Animals↗
PubMed2005

Long-term survival and functional results after aortic valve replacement in asymptomatic patients with chronic severe aortic regurgitation and left ventricular dysfunction.

OBJECTIVES: We examined the influence of medical treatment on the results of surgery in terms of long-term survival and functional results in patients with chronic, severe aortic regurgitation (AR). BACKGROUND: Asymptomatic patients with AR and a reduced left ventricular ejection fraction (LVEF) are at high risk because of a higher-than-expected long-term mortality. The influence of preoperative medical therapy on the outcome after aortic valve replacement (AVR) is not well known. METHODS: Surgery was indicated for the appearance of a reduced LVEF (<50%). At the time of AVR, there were 134 patients treated with nifedipine (group A), and 132 received no medication (group B). RESULTS: Operative mortality was similar in the two groups (0.75% vs. 0.76%, p = NS). The LVEF normalized in all of group A, whereas it remained abnormal in 36 group B patients (28%). At 10-year follow-up, LVEF persisted higher in group A (62 +/- 5% vs. 48 +/- 4%, p < 0.001). Five-year survival was similar in the two groups (94 +/- 2% vs. 94 +/- 3%, p = NS). Group A showed a 10-year survival not different from expected and significantly higher than that in group B (85 +/- 4% vs. 78 +/- 5%, p < 0.001), which had a worse survival than expected. CONCLUSIONS: Unloading treatment with nifedipine in AR allows one to indicate AVR at the appearance of a reduced LVEF with a low operative mortality and an optimal long-term outcome. The concept of surgical correction of AR indicated for reduced LVEF may not be applied to all patients. Indeed, in a large amount of untreated patients, a reduced LVEF preoperatively is not reversed by prompt surgery, indicating irreversible myocardial damage, and 10-year survival is worse than expected.

Adult↗