Cardiovascular magnetic resonance for the diagnosis and management of heart failure with preserved ejection fraction

Heart Failure Reviews - Heart failure with preserved ejection fraction (HFpEF) is characterized by an impaired ventricular filling resulting in the development of dyspnea and other HF symptoms....     

A fast and effective method of quantifying myocardial perfusion by magnetic resonance imaging

The quantification of global myocardial blood flow (MBF) by measuring coronary sinus flow by magnetic resonance (MRI) was demonstrated to be very well correlated with positron emission tomography (PET). We proposed a new method for the quantification of regional myocardial perfusion with MRI by the integration of MBF and first pass technique. The aim of this study was to validate this new method for quantification of regional perfusion by comparing it with 13NH13-PET in swine models of myocardial infarction and in humans in resting and hyperemic conditions. MRI and 13NH3-PET was performed in 2 healthy swine, 11 swine models of myocardial infarction (5 reperfused, 6 non reperfused) and in 12 humans at rest and during hyperemia. MBF was estimated by MRI through the quantification of coronary sinus flow and left ventricular (LV) mass. The upslope of signal intensity (SI-upslope) of each myocardial segment was obtained by the first pass gadolinium technique. Regional SI-upslope was indexed by the upslope of the entire left ventricular myocardium (global upslope). Regional myocardial perfusion was estimated as the product of MBF and SI-upslope/global upslope. Regional perfusion was also estimated by 13NH3-PET. A close agreement of the MRI and PET techniques for measurement of regional myocardial perfusion was found in all myocardial segments by Bland–Altman analysis (mean difference 5.1 %; limits of agreement, ?37.2–27.5 %). With the integration of the first pass technique and the measurement of global MBF by coronary sinus flow/LV mass, MRI allows direct quantification of regional myocardial perfusion.     

Insulin resistance is a major determinant of myocardial blood flow impairment in anginal patients

Purpose

In patients with chest pain, stress-induced myocardial perfusion abnormalities are often the result of depressed myocardial blood flow (MBF) reserve. We investigated the relative contribution of cardiovascular risk factors and coronary atherosclerosis to MBF abnormalities in anginal patients.

Methods

We studied 167 patients with typical (n?=?100) or atypical (n?=?67) chest pain who underwent quantitative evaluation of MBF by PET at rest and after dipyridamole infusion, and quantitative coronary angiography (invasive or by 64-slice CT). Patients with left ventricular (LV) dysfunction (ejection fraction <45 %) were excluded. Coronary atherosclerosis of ≥50 % was defined as obstructive.

Results

At rest median MBF was 0.60 ml min^?1 g^?1, and after dipyridamole infusion median MBF was 1.22 ml min^?1 g^?1. MBF reserve was <2 in 77 of 167 patients (46 %). Coronary atherosclerosis was present in 67 patients (40 %), 26 with obstructive disease. In a univariate analysis several variables were associated with reduced MBF at rest, including male gender, coronary atherosclerosis and elevated LV end-diastolic diameter, and during hyperaemia, including male gender, insulin resistance (IR), smoking habit, LV ejection fraction and end-diastolic diameter. In a multivariate analysis, after adjustment for LV function and for pharmacological treatments, male gender was the only independent predictor of reduced MBF at rest (P?<?0.001), while male gender (P?=?0.003), IR (P?=?0.033) and coronary atherosclerosis (P?<?0.001) remained the only independent predictors of reduced hyperaemic MBF. IR (P?=?0.043) and coronary atherosclerosis (P?=?0.005) were the only predictors of depressed MBF reserve. Coronary atherosclerosis, male gender and IR showed additive effects on hyperaemic MBF.

Conclusion

In patients with chest pain and normal LV systolic function, IR, male gender and coronary atherosclerosis are independent and additive determinants of impaired hyperaemic MBF.