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Biomedical subjects

Christopher M Kramer

Publications and source records attributed to Christopher M Kramer.

44 records · Page 3Linked to original sources
PubMed2002

Angiotensin II type 2 receptor overexpression preserves left ventricular function after myocardial infarction.

BACKGROUND: The role of the angiotensin II type 2 receptor (AT2-R) in left ventricular (LV) remodeling may depend on the underlying stimulus. We hypothesized that cardiac AT2-R overexpression in transgenic (TG) mice would attenuate remodeling after myocardial infarction (MI). METHODS AND RESULTS: Ten wild-type (WT) C57BL/6 mice and 12 TG mice that overexpress the AT2-R in the heart were studied by cardiac MRI at baseline and days 1, 7, and 28 post-MI induced by 1 hour of occlusion of the LAD followed by reperfusion. Short-axis imaging from apex to base was used to determine LV mass index, end-diastolic and end-systolic volume indices (EDVI, ESVI), regional wall thickness and thickening, and ejection fraction (EF). Gadolinium-DTPA was infused 20 minutes before day 1 imaging to assess infarct size. At baseline, heart rate, blood pressure, LV mass index, and EDVI were similar between groups. Baseline ESVI was lower (0.20+/-0.07 versus 0.45+/-0.15 microL/g, P<0.001) and EF higher (82.3+/-4.9% versus 67.7+/-5.3%, P<0.001) in TG than WT. Infarct size was similar (36.6+/-7.2% in WT, 34.0+/-7.8% in TG, P=NS). When controlled for baseline differences, ESVI was significantly less and EF significantly higher at all time points in TG versus WT. At day 28, ESVI was 1.05+/-0.32 microL/g in TG and 1.63+/-0.41 microL/g in WT, P<0.03, and EF was 47.3+/-5.8% versus 34.1+/-9.2%, P<0.003, respectively. Regional wall thickness and thickening were greater in TG both at baseline and at day 28. At day 28, blood pressure and LV dP/dt were higher in TG. CONCLUSIONS: Cardiac AT2-R overexpression improves LV systolic function at baseline and preserves function during post-MI remodeling.

Animals↗
PubMed2002

MR tagging early after myocardial infarction in mice demonstrates contractile dysfunction in adjacent and remote regions.

The purpose of this study was to use MR myocardial tagging to assess regional cardiac function after myocardial infarction (MI) in mice. Eight mice were imaged before and 1 day after MI. MRI included cine imaging, myocardial tagging, and contrast-enhanced imaging. Regional percent circumferential shortening (%CS) was measured from the tagged images, and the region of hyperenhancement on the contrast-enhanced images was used to determine the infarcted, adjacent, and remote zones. Ejection fraction (EF) fell from 59% +/- 6% at baseline to 32% +/- 6% after MI (P < 0.01). At baseline, %CS was 14.5% +/- 3.4%. After MI, %CS was 0.7% +/- 4.4% in the infarcted zone, 7.4% +/- 4.4% in the adjacent zone, and 11.8% +/- 4.2% in the remote zone. %CS was statistically different for all comparisons between the infarcted, adjacent, remote, and baseline groups (P < 0.01). MR tagging can detect regional differences in myocardial function post-MI in mice.

Animals↗
PubMed2002

Altered excitation-contraction coupling in myocytes from remodeled myocardium after chronic myocardial infarction.

Following myocardial infarction (MI), the left ventricle undergoes progressive dilatation and eccentric hypertrophy, i.e., remodeling, which is greater in the adjacent than the remote region. The cellular mechanisms underlying these regional differences were studied. One (n=5) and 8 weeks (n=8) after anteroapical MI in sheep, cardiac myocytes were isolated from the adjacent and remote regions. At 8 weeks after MI, myocyte function in the remote region was not different from values either in sham controls (n=3) or animals 1 week after MI. At 8 weeks after MI, myocyte contractile function (% contraction) was decreased, P<0.01, in the adjacent region (6.4+/-0.4%), as compared with the remote region (8.8+/-0.5%) and was associated with decreased amplitude of Ca(2+)transients (adjacent, 0.69+/-0.09 v remote, 1.08+/-0.20, P<0.05) and L-type Ca(2+)current density (adjacent, 3.6+/-0.2 v remote, 4.8+/-0.2 pA/pF, P<0.05). Relaxation was also impaired significantly in myocytes from the adjacent region, associated with decreased protein levels of SERCA2a. The myocytes were hypertrophied more in the adjacent region than the remote region. Furthermore, focal areas of central myofibrillar lysis and increased glycogen deposition were observed in the adjacent region. These results indicate that impaired excitation-contraction coupling underlies dysfunction of myocytes from the adjacent non-infarcted myocardium after chronic MI, even in the absence of heart failure. Hypertrophy is implicated as the mechanism, since these changes were noted at 8 weeks, but not at 1 week after MI.

Animals↗
PubMed2002

MR imaging of atherosclerotic plaque.

MRI is a powerful noninvasive imaging tool with high spatial resolution that continues to prove its value in determining atherosclerotic plaque size, volume, and tissue components. Multispectral MRI sequences have been validated to characterize atherosclerotic plaque components in animals; they have recently been applied to human aorta and carotid artery and are being used to identify the vulnerable plaque. The ability to measure wall thickness in human coronary artery wall has been realized. Future developments may allow plaque characterization in the coronary arteries with surface coil imaging, but intravascular MRI may play an important role in this regard. Novel contrast agents for identifying inflammation and thrombus within atherosclerotic plaque will aid in the identification of higher-risk atherosclerotic disease. Lastly, MRI has progressed to the point where it can be used in serial studies of atherosclerotic plaque progression and regression in the face of therapeutic intervention. MRI will continue to evolve an important role in imaging of atherosclerotic plaque.

Animals↗
PubMed2002

Magnetic resonance tagging and echocardiographic response to dobutamine and functional improvement after reperfused myocardial infarction.

OBJECTIVE: Our objective was to compare the qualitative response to low-dose dobutamine by echocardiography (DSE) with the quantitative response of magnetic resonance myocardial tagging (DMRT) in the prediction and evaluation of functional improvement after reperfused myocardial infarction (MI). METHODS: Twenty-two patients with a reperfused first MI (aged 51 +/- 2 years, 20 male, 13 anterior MI) were studied. On day 3 +/- 1 after MI, patients underwent both DSE and DMRT at baseline and during infusion of 5 microg/kg/min and 10 microg/kg/min of dobutamine. The patients returned at week 8 +/- 1 for follow-up echocardiogram and MRT at rest. Two experienced observers interpreted the DSE for the presence of contractile reserve and functional improvement in dysfunctional segments. By DMRT, a 5% increase in percent intramyocardial circumferential shortening at peak response to dobutamine was defined as evidence of contractile reserve. Functional improvement by echocardiography was defined as the gold standard. RESULTS: Ejection fraction improved from 46% +/- 10% at week 1 to 51% +/- 12% at week 8 (P <.001) in the patients. Sixty-seven transmural segments with baseline dysfunction matched between imaging modalities by location were studied. For 51 (76%) of the segments, echocardiography and MR tagging were concordant in the assessment of functional improvement (kappa value 0.52). Twenty-nine segments (43%) demonstrated improvement by echocardiography, whereas 33 segments (49%) improved by MR tagging. With improvement of function by echocardiography as gold standard, the sensitivity and specificity of DMRT for prediction of functional improvement was 86% and 69%, respectively, with an overall accuracy of 76%. The sensitivity, specificity, and accuracy of DSE was 86%, 87%, and 85%, respectively. Overall accuracy was similar between techniques. CONCLUSIONS: Both DSMRT and DSE are sensitive and accurate techniques for predicting functional improvement after reperfused MI.

Cardiotonic Agents↗
PubMed2002

Reverse remodeling and improved regional function after repair of left ventricular aneurysm.

BACKGROUND: Changes in regional left ventricular mechanics after anteroapical aneurysm repair in human subjects can be studied noninvasively by means of magnetic resonance tagging. We hypothesized that left ventricular intramyocardial function would improve throughout the left ventricle after repair. METHODS: We studied 6 male patients with a left ventricular anteroapical aneurysm (mean age +/- SD, 63 +/- 5 years) using magnetic resonance tagging 3 +/- 1 weeks before and 6 +/- 1 weeks after aneurysm repair, coronary artery bypass grafting, and mitral valve repair (n = 2). Breath-hold tagged imaging spanned the left ventricle in the short axis from apex to base. Left ventricular mass, end-diastolic and end-systolic volume, and ejection fraction were measured. Two-dimensional strain analysis was applied; averaged for the apical, middle, and basal left ventricle and the whole left ventricle; and expressed as greatest lengthening (similar to wall thickening), greatest shortening, and angular deviation of the lengthening strain from the radial direction. RESULTS: After aneurysm repair, left ventricular mass decreased from 373 +/- 27 to 333 +/- 25 g (P <.05), end-diastolic volume from 212 +/- 22 to 168 +/- 18 mL (P <.005), and end-systolic volume from 188 +/- 26 to 113 +/- 18 mL (P <.005); ejection fraction improved from 13% +/- 4% to 23% +/- 4% (P <.005). For the whole left ventricle, lengthening strain increased from before to after the operation (8% +/- 1% to 10% +/- 1%, P <.01). Most of the improved lengthening occurred at the middle left ventricle (8% +/- 1% to 11% +/- 1%, P <.01), in the base (8% +/- 1% to 10% +/- 1%, P <.05), and in the inferior wall (9% +/- 1% to 12% +/- 1%, P <.05). Lengthening tended to become more radially oriented, decreasing from 31 degrees +/- 3 degrees to 27 degrees +/- 3 degrees (P =.10). Shortening strain did not change (10% +/- 1% to 11% +/- 1%, P = not significant). CONCLUSIONS: Left ventricular aneurysm repair is associated with reverse remodeling and an improvement in the extent and orientation of intramyocardial function, especially at the middle and basal left ventricle and inferior wall.

Adult↗
PubMed2002

Fully automated registration and warping of contrast-enhanced first-pass perfusion images.

Respiratory motion during acquisition of first-pass myocardial perfusion images results in translation, distortion from out-of-plane motion, and changes in left ventricular geometry. Together these effects make visual image analysis more difficult and limit methods of quantitative analysis of contrast kinetics. We present a fully automated registration and warping algorithm for correcting translation and geometric distortions using a statistically based image registration method. Twelve patients (mean age 51 +/- 12 years) were studied 3 +/- 1 days after reperfused first myocardial infarction. Perfusion images were acquired during bolus administration of nonionic Gd-DTPA. Pixel intensity statistics were computed for each image in the neighborhood of high spatial frequencies. These statistics were then used to register and warp each target image (image to be registered and warped) to a common template image. Average image-to-image vertical translation was 2.6 +/- 0.8 pixels (3.4 +/- 1.0 mm) prior to processing and 0.9 +/- 0.3 pixels (1.2 +/- 0.4 mm) post-processing (P < 0.0001). Mean image-to-image horizontal translation was 1.7 +/- 1.2 pixels (1.8 +/- 1.2 mm) before and 1.3 +/- 0.7 pixels (1.4 +/- 0.7 mm) after processing (P = 0.05). Left ventricular endocardial area varied an average of 105 +/- 55 pixels (140.7 +/- 53.7 mm2) between images prior to processing vs. 51 +/- 15 pixels (68.3 +/- 20.1 mm2) after processing (P < 0.001). Thus automated, statistically based registration and warping of perfusion images is effective in reducing image-to-image translation. This method may permit more sensitive qualitative and quantitative evaluation of myocardial contrast-enhanced first-pass images.

Algorithms↗