Cardiac magnetic resonance imaging safety following percutaneous coronary intervention.

In the first 8 weeks after percutaneous coronary intervention (PCI), possible negative interactions exist between the cardiac magnetic resonance (CMR) imaging environment and the weakly ferromagnetic material in coronary stents. There are circumstances when CMR would be indicated shortly following PCI, such as acute myocardial infarction (AMI). The purpose of this study is to demonstrate CMR safety shortly following stent PCI in AMI patients. We performed a retrospective analysis of safety data in AMI patients with recently placed coronary artery stents enrolled in a multi-center phase II trial for gadoversetamide. Patients underwent 1.5 T CMR within 16 days of PCI. Vital signs (blood pressure, heart rate, respiratory rate, and body temperature) and ECGs were taken pre-CMR, 1, 2, and 24 h post-CMR. Any major adverse cardiac event (MACE) or other serious adverse events in the first 24 h after MRI were recorded. There were 258 stents in 211 AMI patients. The mean delay to CMR following PCI was 6.5 ± 4 days, with 62 patients (29 %) receiving CMR within 3 days and 132 patients (63 %) within 1 week. Patients showed no significant vital sign changes following CMR. Ten patients (4.7 %) showed mild, transient ECG changes. Within the 24-h follow-up group, 4 patients (1.9 %) had moderate to severe events, including chest pain (1) and elevated cardiac enzymes (1), resolving in 24 h; heart failure (1) and ischemic stroke (1). There were no deaths. This study demonstrates fewer MACE in AMI patients undergoing 1.5 T CMR within 16 days of stent placement in comparison to post-stent event rate reported in the literature. This study adds to the CMR after stent PCI safety profile suggested by previous studies and is the largest and first study that uses multicenter data to assess stent safety following CMR examination.

Quantification of global myocardial oxygenation in humans: initial experience.

PURPOSE: To assess the feasibility of our newly developed cardiovascular magnetic resonance (CMR) methods to quantify global and/or regional myocardial oxygen consumption rate (MVO2) at rest and during pharmacologically-induced vasodilation in normal volunteers. METHODS: A breath-hold T2 quantification method is developed to calculate oxygen extraction fraction (OEF) and MVO2 rate at rest and/or during hyperemia, using a two-compartment model. A previously reported T2 quantification method using turbo-spin-echo sequence was also applied for comparison. CMR scans were performed in 6 normal volunteers. Each imaging session consisted of imaging at rest and during adenosine-induced vasodilation. The new T2 quantification method was applied to calculate T2 in the coronary sinus (CS), as well as in myocardial tissue. Resting CS OEF, representing resting global myocardial OEF, and myocardial OEF during adenosine vasodilation were then calculated by the model. Myocardial blood flow (MBF) was also obtained to calculate MVO2, by using a first-pass perfusion imaging approach. RESULTS: The T2 quantification method yielded a hyperemic OEF of 0.37 +/- 0.05 and a hyperemic MVO2 of 9.2 +/- 2.4 micromol/g/min. The corresponding resting values were 0.73 +/- 0.05 and 5.2 +/- 1.7 micromol/g/min respectively, which agreed well with published literature values. The MVO2 rose proportionally with rate-pressure product from the rest condition. The T2 sensitivity is approximately 95% higher with the new T2 method than turbo-spin-echo method. CONCLUSION: The CMR oxygenation method demonstrates the potential for non-invasive estimation of myocardial oxygenation, and should be explored in patients with altered myocardial oxygenation.

PET detection of the impact of dobutamine on myocardial glucose metabolism in women with type 1 diabetes mellitus.

BACKGROUND: Our objective was to determine, in the hearts of women with type 1 diabetes mellitus (T1DM), whether the fate of extracted glucose is altered and, if so, what the impact of dobutamine is on myocardial substrate metabolism. In experimental models of T1DM, myocardial glycolysis and glucose oxidation are reduced with the impairment becoming more pronounced with dobutamine. Whether similar changes occur in humans with T1DM is unclear. METHODS AND RESULTS: Myocardial perfusion, oxygen consumption, and glucose and fatty acid metabolism were measured with positron emission tomography in 19 women, 7 normal volunteers (NVs) and 12 with T1DM. The NVs and 6 T1DM (DM1) patients were studied under baseline metabolic conditions and 6 T1DM patients were studied during hyperinsulinemic-euglycemic clamp (DM1-C), both at rest and during dobutamine. At rest, myocardial glucose uptake, glycolysis, glycogen storage, and oxidation were reduced by similar levels in DM1 patients compared with NVs (P < .05). During dobutamine, although myocardial glucose uptake was not different from DM1 patients at rest, fractional glycolysis was lower compared with NVs or DM1-C patients and reflected a lower glucose oxidation rate (P < .001). Measurements of myocardial glucose metabolism at rest and during dobutamine were comparable between NVs and DM1-C patients. During dobutamine, myocardial fatty acid uptake and oxidation increased in all 3 groups. CONCLUSIONS: In women with T1DM, (1) myocardial glucose metabolism is impaired downstream from initial uptake, (2) these abnormalities become more pronounced with dobutamine and are paralleled by an increase in myocardial fatty acid metabolism, and (3) insulin restores glucose metabolism to levels observed in normal control subjects.

Fatty acids and insulin modulate myocardial substrate metabolism in humans with type 1 diabetes.

OBJECTIVE: Normal human myocardium switches substrate metabolism preference, adapting to the prevailing plasma substrate levels and hormonal milieu, but in type 1 diabetes, the myocardium relies heavily on fatty acid metabolism for energy. Whether conditions that affect myocardial glucose use and fatty acid utilization, oxidation, and storage in nondiabetic subjects alter them in type 1 diabetes is not well known. RESEARCH DESIGN AND METHODS: To test the hypotheses that in humans with type 1 diabetes, myocardial glucose and fatty acid metabolism can be manipulated by altering plasma free fatty acid (FFA) and insulin levels, we quantified myocardial oxygen consumption (MVo(2)), glucose, and fatty acid metabolism in nondiabetic subjects and three groups of type 1 diabetic subjects (those studied during euglycemia, hyperlipidemia, and a hyperinsulinemic-euglycemic clamp) using positron emission tomography. RESULTS: Type 1 diabetic subjects had higher MVo(2) and lower myocardial glucose utilization rate/insulin than control subjects. In type 1 diabetes, glucose utilization increased with increasing plasma insulin and decreasing FFA levels. Myocardial fatty acid utilization, oxidation, and esterification rates increased with increasing plasma FFA. Increasing plasma insulin levels decreased myocardial fatty acid esterification rates but increased the percentage of fatty acids going into esterification. CONCLUSIONS: Type 1 diabetes myocardium has increased MVo(2) and is insulin resistant during euglycemia. However, its myocardial glucose and fatty acid metabolism still responds to changes in plasma insulin and plasma FFA levels. Moreover, insulin and plasma FFA levels can regulate the intramyocardial fate of fatty acids in humans with type 1 diabetes.

Increased myocardial fatty acid metabolism in patients with type 1 diabetes mellitus.

OBJECTIVES: The purpose of this study was to determine if myocardial fatty acid utilization (MFAU) and myocardial fatty acid oxidation (MFAO) are increased in diabetic patients. BACKGROUND: Experimental models of diabetes mellitus demonstrate that MFAU and MFAO are increased, and that this dependence on myocardial fatty acid metabolism may be detrimental to cardiac function. Whether similar metabolic changes occur in humans with diabetes mellitus is unclear. METHODS: Eleven healthy non-diabetic control patients (5 women, ages 25 +/- 5 years) and 11 otherwise healthy patients with type 1 diabetes mellitus (T1DM) (8 women, ages 36 +/- 10 years, HbA1c 8.4 +/- 1.9%) underwent positron emission tomography for the determination of myocardial blood flow (MBF); myocardial oxygen consumption (MVO2); myocardial glucose utilization (MGU); and MFAU, MFAO, and %MFAO. RESULTS: Plasma lactate, insulin, and MBF levels were similar between the two groups. However, plasma glucose (5.71 +/- 0.98 mumol/ml vs. 5.28 +/- 0.65 mumol/ml, p = 0.04), free fatty acid levels (0.60 +/- 0.24 mumol/ml vs. 0.19 +/- 0.07 mumol/ml, p < 0.0001), and MVO2 (6.64 +/- 2.21 vs. 4.51 +/- 1.39 mumol/g/min, p = 0.007) levels were higher in the T1DM subjects. Furthermore, compared with control patients, T1DM subjects exhibited higher MFAU (213 +/- 135 nmol/g/min vs. 57 +/- 28 nmol/g/min, p = 0.0004), MFAO (206 +/- 131 nmol/g/min s. 50 +/- 26 nmol/g/min, p = 0.0002), and %MFAO (94 +/- 6% vs. 81 +/- 19%, respectively, p = 0.04). In contrast, MGU was lower in T1DM subjects than in controls (207 +/- 108 nmol/g/min vs. 403 +/- 191 nmol/g/min, p = 0.0008). CONCLUSIONS: Humans with diabetes mellitus exhibit increased MFAU and MFAO and reduced MGU consistent with observations obtained in experimental models of diabetes.

The effects of plasma insulin and glucose on myocardial blood flow in patients with type 1 diabetes mellitus.

OBJECTIVES: The objective of this study was to determine the impact of insulin and glucose on myocardial vasodilator function in patients with type 1 diabetes mellitus (T1DM). BACKGROUND: The relative importance of plasma insulin and glucose levels on the abnormal vasodilator function observed in T1DM is unknown. METHODS: Twenty T1DM patients underwent positron emission tomography studies to measure myocardial blood flow (MBF) (in ml/g/min) at rest (MBFr) and during adenosine (MBFa), both under baseline metabolic conditions and then during either hyperinsulinemic-euglycemic clamp (HE) (n = 10; 40 +/- 9 years, 8 female subjects, hemoglobin A1c [HbA1c] 7.8 +/- 1.1%) or hyperinsulinemic-hyperglycemic clamp (HH) (n = 10; 44 +/- 12 years, 8 female subjects, hemoglobin A1c 7.7 +/- 0.6%). RESULTS: Both groups showed similar MBFr and MBFa under baseline metabolic conditions (p = NS). Compared with baseline conditions, MBFr increased in the HH group (p < 0.005), whereas it did not change in the HE group. Compared with baseline conditions, MBFa decreased in the HH group (p < 0.05) but did not change in the HE group. Myocardial perfusion reserve (MPR) (MBFa/MBFr) was similar between the HE and HH groups at baseline (p = NS). During clamp, MPR tended to decrease in the HH group (p < 0.1) but did not change in the HE group (p = NS) when compared with baseline conditions. However, during the clamp MPR was significantly lower in the HH group when compared with the HE group (p < 0.0001). CONCLUSIONS: In the short term, hyperglycemia has a deleterious effect on myocardial vasodilator function, which outweighs the beneficial effect of hyperinsulinemia.