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N Reichek

Publications and source records attributed to N Reichek.

At least 37 records · Page 2Linked to original sources

Beta-blockade improves adjacent regional sympathetic innervation during postinfarction remodeling.

The effect of beta-blockade on left ventricular (LV) remodeling, when added to angiotensin-converting enzyme inhibition (ACEI) after anterior myocardial infarction (MI), is incompletely understood. On day 2 after coronary ligation-induced anteroapical infarction, 17 sheep were randomized to ramipril (ACEI, n = 8) or ramipril and metoprolol (ACEI-beta, n = 9). Magnetic resonance imaging was performed before and 8 wk after MI to measure changes in LV end-diastolic, end-systolic, and stroke volume indexes, LV mass index, ejection fraction (EF), and regional percent intramyocardial circumferential shortening. (123)I-labeled m-iodobenzylguanidine (MIBG) and fluorescent microspheres before and after adenosine were infused before death at 8 wk post-MI for quantitation of sympathetic innervation, blood flow, and blood flow reserve in adjacent and remote noninfarcted regions. Infarct size, regional blood flow, blood flow reserve, and the increase in LV mass and LV end-diastolic and end-systolic volume indexes were similar between groups. However, EF fell less over the 8-wk study period in the ACEI-beta group (-13 +/- 11 vs. -22 +/- 4% in ACEI, P < 0.05). The ratio of adjacent to remote region (123)I-MIBG uptake was greater in ACEI-beta animals than in the ACEI group (0.93 +/- 0.06 vs. 0.86 +/- 0.07, P < 0.04). When added to ACE inhibition after transmural anteroapical MI, beta-blockade improves EF and adjacent regional sympathetic innervation but does not alter LV size.

Adrenergic beta-Antagonists↗

Quantitative assessment of myocardial viability after infarction by dobutamine magnetic resonance tagging.

BACKGROUND: The assessment of return of function within dysfunctional myocardium after acute myocardial infarction (MI) using contractile reserve has been primarily qualitative. Magnetic resonance (MR) myocardial tagging is a novel noninvasive method that measures intramyocardial function. We hypothesized that MR tagging could be used to quantify the intramyocardial response to low-dose dobutamine and relate this response to return of function in patients after first MI. METHODS AND RESULTS: Twenty patients with a first reperfused MI (age, 53+/-12 years; 16 male; 11 inferior MIs) were studied. Patients underwent breath-hold MR-tagged short-axis imaging on day 4+/-2 after MI at baseline and during dobutamine infusion at 5 and 10 microg x kg(-1) x min(-1). At 8+/-1 weeks after MI, patients returned for a follow-up MR tagging study without dobutamine. Quantification of percent intramyocardial circumferential segment shortening (%S) was performed. Low-dose dobutamine MRI was well tolerated. Overall, mean %S was 15+/-11% at baseline (n=227 segments), increased to 16+/-10% at 5 microg x kg(-1) x min(-1) dobutamine (P=NS), 21+/-10% at peak (P<0.0001 versus baseline and 5 microg x kg(-1) x min(-1), and 18+/-10% at 8 weeks (P<0.004 versus baseline and peak). The increase in %S with peak dobutamine was greater in dysfunctional myocardium (103 segments, +9+/-10%) than in normal tissue (124 segments, +4+/-12%, P<0.0001). In dysfunctional regions, %S also increased from 6+/-7% at baseline to 14+/-10% at 8 weeks after MI (P<0.0001). In dysfunctional regions that responded normally to peak dobutamine (> or =5% increase in %S), the increase in %S from baseline to 8 weeks after MI (+9+/-9%) was greater than in those regions that did not respond normally (+5+/-9%, P<0.04). Midmyocardial and subepicardial response to dobutamine were predictive of functional recovery, but the subendocardial response was not. CONCLUSIONS: The response of intramyocardial function to low-dose dobutamine after reperfused MI can be quantified with MR tagging. Dysfunctional tissue after MI demonstrates a larger contractile response to dobutamine than normal myocardium. A normal increase in shortening elicited by dobutamine within dysfunctional midwall and subepicardium predicts greater functional recovery at 8 weeks after MI, but the response within the subendocardium is not predictive.

Adult↗

Regional myocyte hypertrophy parallels regional myocardial dysfunction during post-infarct remodeling.

After large myocardial infarction (MI), left-ventricular (LV) remodeling is characterized by cavity dilatation, eccentric hypertrophy, and regional mechanical dysfunction. We wished to correlate cellular hypertrophy chronically after MI with in vivo function on a regional basis within non-infarcted myocardium. Twelve sheep were studied. Seven underwent coronary ligation to create an anteroapical MI. Magnetic resonance imaging (MRI) was performed once in controls, and prior to and 8 weeks after infarction, for measurement of LV mass, volumes, ejection fraction, and regional intramyocardial circumferential shortening (%S). Myocyte morphometric indices (cell volume, length, cross-sectional area, width, and length/width ratios) were measured from myocytes isolated from regions adjacent to (within 2 cm of the infarct border) and remote from the infarct and at corresponding loci in the control animals. From baseline to 8 weeks after infarction in the infarcted animals, end-diastolic volume increased from (mean+/-s.d.) 1.9+/-0.4 ml/kg to 2.6+/-0.4 ml/kg (P<0.02) and EF fell from 49+/-6 to 35+/-6% (P<0.02). LV mass trended upwards from 2.2+/-0.4 to 2.6+/-0.4 g/kg (P=n.s.). Regionally, %S in the region adjacent to the infarct fell (from 19+/-3 to 13+/-3%, P<0.003) while remote %S did not change. Cell volume in adjacent non-infarcted regions was greater than that in remote non-infarcted regions (3.8+/-0.9x10(4) micrometer3 v 2.6+/-0. 8x10(4) micrometer3, P<0.006) and this difference (+1.2+/-0.7x10(4) micrometer3) was greater than the corresponding regional difference in controls (+0.4+/-0.2x10(4) micrometer3, P<0.05). Similarly, myocytes in adjacent non-infarcted regions were longer (138.0+/-10.1 micrometer) than in remote regions (123.7+/-10.1 micrometer, P<0.002), and this difference (+14.3+/-7.2 micrometer) was greater than that in controls (-1.4+/-5.6 micrometer, P<0.003). Adjacent %S correlated inversely with adjacent myocyte cell volume (r=-0.72, P<0.009) and cell length (r=-0.70, P<0.02). In mechanically dysfunctional non-infarcted regions adjacent to chronic transmural myocardial infarction in the remodeled LV, disproportionate cellular hypertrophy occurs, predominantly due to an increase in cell length. Mechanical dysfunction in these regions correlates with cell lengthening and hypertrophy.

Animals↗

Vessel boundary extraction based on a global and local deformable physical model with variable stiffness.

Reliable and efficient vessel cross-sectional boundary extraction is very important for many medical magnetic resonance (MR) image studies. General purpose edge detection algorithms often fail for medical MR images processing due to fuzzy boundaries, inconsistent image contrast, missing edge features, and the complicated background of MR images. In this regard, we present a vessel cross-sectional boundary extraction algorithm based on a global and local deformable model with variable stiffness. With the global model, the algorithm can handle relatively large vessel position shifts and size changes. The local deformation with variable stiffness parameters enable the model to stay right on edge points at the location where edge features are strong and at the same time, fit a smooth contour at the location where edge features are missing. Directional gradient information is used to help the model to pick correct edge segments. The algorithm was used to process MR cine phase-contrast images of the aorta from 20 volunteers (over 500 images) with excellent results.

Algorithms↗

Transient ischemia does not limit subsequent ischemic regional dysfunction in humans: a transesophageal echocardiographic study during minimally invasive coronary artery bypass surgery.

OBJECTIVES: This study sought to assess the effects of sequential coronary artery occlusion during minimally invasive coronary artery bypass graft surgery (CABG) on hemodynamic variables and left ventricular systolic function by means of transesophageal echocardiography (TEE). BACKGROUND: Clinical and experimental studies suggest a protective effect of ischemic preconditioning in patients with acute coronary syndromes. However, the effect of repetitive myocardial ischemia on myocardial mechanical function in humans is not completely understood. METHODS: Seventeen patients with left anterior descending coronary artery (LAD) stenosis > or =70% and normal rest left ventricular systolic function referred for minimally invasive CABG underwent intraoperative TEE for assessment of regional left ventricular wall motion and measurement of hemodynamic variables at baseline (baseline 1), during a 5-min coronary occlusion (occlusion 1), after a 5-min reperfusion period (baseline 2) and a during a second coronary occlusion during bypass anastomosis (occlusion 2). RESULTS: Left ventricular wall motion score (LVWMS) increased significantly from baseline (16.0) to occlusion 1 (21.4+/-3.1 [mean +/- SD], p < 0.05) and occlusion 2 (21.8+/-3.1, p < 0.05). No difference in LVWMS was noted between occlusions 1 and 2. Pulmonary artery systolic pressure increased significantly from baseline (25+/-6 mm Hg) to occlusion 1 (32+/-7 mm Hg, p < 0.05) and occlusion 2 (33+/-6 mm Hg, p < 0.05). Pulmonary artery diastolic pressure also increased significantly from baseline (12+/-4 mm Hg) to occlusion 1 (16+/-4 mm Hg, p < 0.05) and occlusion 2 (16+/-4 mm Hg, p < 0.05). No significant differences in pulmonary artery pressures were noted between occlusions 1 and 2. CONCLUSIONS: Ischemic dysfunction was precipitated by the 5-min LAD occlusion, as shown by the increase in LVWMS and pulmonary artery pressure. However, a 5-min coronary occlusion and the resulting ischemia do not alter regional left ventricular systolic function during subsequent ischemia in humans.

Aged↗

Multiplane transesophageal echocardiographic identification of the involved scallop in patients with flail mitral valve leaflet: intraoperative correlation.

Although the role of multiplane transesophageal echocardiography in the diagnosis of flail mitral valve leaflet is well described, the accuracy of this modality in localizing the involved posterior leaflet scallop (medial, middle, or lateral) has never been validated. For 54 patients undergoing intraoperative transesophageal echocardiography for severe mitral regurgitation due to flail mitral valve leaflet, we assessed the accuracy of a systematic approach to localization of the flail mitral valve leaflet. Surgical confirmation was performed for all patients. At blinded review, a sensitivity of 78%, specificity of 92%, and overall diagnostic accuracy of 88% were achieved for correct localization of the flail posterior leaflet scallop. The middle scallop was most commonly affected in this series. The medial scallop was affected least often, and diagnosis of lesions in that area was least accurate. This diagnostic approach appears to be accurate and feasible and may assist in planning specific surgical therapy for this disorder.

Adult↗

Breath-hold dobutamine magnetic resonance myocardial tagging: normal left ventricular response.

Analysis of the changes in myocardial deformation produced by adrenergic stress has been limited by the imaging techniques used. We used rapid magnetic resonance imaging (MRI) myocardial tagging to map the dose-dependent response to incremental dobutamine in the normal human left ventricle. Thirteen volunteers underwent breath-hold tagged cine MRI during dobutamine infusion. Images were acquired throughout systole to a peak dose of 20 microg/kg/min. End-systolic percent circumferential shortening (%S) was measured at 3 transmural locations and 4 circumferential locations at 3 long-axis positions. Mean circumferential shortening velocity (CSV) was also calculated at each location and dose. Mean %S reached a maximum of 26 +/- 3% at 10 microg/kg/min compared with 21 +/- 4% at baseline (p <0.003). Peak %S was reached by 10 microg/kg/min before a significant increase in heart rate or blood pressure and was unchanged at higher doses. In contrast, CSV increased linearly with dobutamine dose from 4.4 +/- 0.9 mm/s at baseline to 9.8 +/- 1.4 mm/s at 20 microg/kg/min (p <0.0001). Breath-hold tagged dobutamine MRI is safe and effective in detecting regional and transmural changes in function during incremental dobutamine. CSV increased continuously across the dobutamine dose range. At low dose (< or =10 microg/kg/min) %S increased without any change in blood pressure or heart rate. Maintenance of peak %S beyond 10 microg/kg/min in the presence of decreasing systolic intervals resulted from a continued increase in CSV. Thus, CSV may be the preferred measure of contractile function during dobutamine stimulation in human myocardium.

Adrenergic beta-Agonists↗

Usefulness of magnetic resonance imaging early after acute myocardial infarction.

In patients, early after acute myocardial infarction (AMI), rapid magnetic resonance imaging (MRI) techniques have been used to assess left ventricular (LV) structure, global and regional function, infarct artery patency, or contrast uptake individually. We hypothesized that MRI could be used as a comprehensive evaluation of the post-AMI patient, studying all of these parameters in < 1 hour. Twenty-seven patients were studied after first AMI. Complete examinations were performed in 23 patients, 16 with anterior and 7 with inferior wall myocardial infarction, on day 5 +/- 2 after the event. For measurement of LV structure and regional function, a breath-hold segmented k-space gradient echo tagging sequence was used. A fat-suppressed segmented k-space breath-hold sequence was used for coronary artery imaging. MRI contrast-enhanced images during bolus gadoteridol transit through the myocardium were obtained to assess first-pass contrast uptake. No adverse events were noted during the MRI scanning, which was completed in 46 +/- 5 minutes. The LV mass index, end-diastolic and end-systolic volume indexes, and ejection fraction were (mean +/- SD) 107 +/- 13 g/m2, 87 +/- 23 ml/m2, 54 +/- 20 ml/m2, and 39 +/- 12%, respectively. Intramyocardial percent circumferential shortening was 11 +/- 6% at the apex, 14 +/- 4% in the midventricle, and 15 +/- 4% at the base. Flow within all infarct arteries was visualized. Seventeen of 23 patients had regions of reduced contrast uptake on first-pass imaging with mean signal intensity of 47 +/- 24% that of remote regions. In patients with recent AMI, comprehensive assessment of LV structure and function, infarct artery patency, and regional myocardial contrast uptake was safe and feasible with MRI of < 1 hour.

Adult↗

Correlations between coronary flow reserve measured with a Doppler guide wire and treadmill exercise testing.

We compared exercise test results to a physiologic depiction of stenosis severity, coronary flow reserve (CFR), measured with a Doppler guide wire in 35 patients with single-vessel coronary disease. Group 1 (n = 21) had abnormal CFR, and group 2 (n = 14) had normal CFR. In group 1, 14 of 21 had ST-segment depression versus 3 of 14 in group 2 (p < 0.01). Exercise treadmill time (Bruce protocol) was normalized to the age- and sex-predicted time. Exercise time and normalized exercise time were less in group 1 (5.6 +/- 2.3 vs 9.9 +/- 1.8 min and 0.82 +/- 0.32 vs 1.25 +/- 0.23, p < 0.00001). Having either ST-segment depression or a normalized exercise time <1 during exercise had a 95% sensitivity, 71% specificity, and 86% predictive accuracy in identifying abnormal CFR. Coronary stenoses and minimal lumen diameter were similar in groups 1 and 2. By using stepwise logistical regression analysis, exercise time and ST-segment depression predicted CFR with a total r2 of 0.51. Minimal lumen diameter did not significantly add to the model. Exercise test variables, ST-segment depression, and exercise time are predictive of the physiologic significance of coronary lesions.

Aged↗

Reduced sympathetic innervation underlies adjacent noninfarcted region dysfunction during left ventricular remodeling.

OBJECTIVES: We examined the association of sympathetic denervation and reduced blood flow with mechanical dysfunction in adjacent noninfarcted regions late after myocardial infarction (MI). BACKGROUND: Using a well characterized ovine model of left ventricular (LV) remodeling after transmural anteroapical MI, we previously showed that histologically normal adjacent noninfarcted regions demonstrate mechanical dysfunction. METHODS: Ten sheep underwent coronary ligation. Magnetic resonance imaging was performed before and 8 weeks after infarction for measurement of LV mass, volumes, ejection fraction and regional intramyocardial circumferential shortening (%S). Iodine-123 metaiodobenzylguanidine (I-123 MIBG) and fluorescent microspheres before and after administration of adenosine were infused before death for measurement of sympathetic innervation, blood flow and blood flow reserve from matched postmortem regions. RESULTS: From baseline to 8 weeks after infarction, LV end-diastolic volume increased from (mean +/- SD) 1.5 +/- 0.3 to 2.6 +/- 0.5 ml/kg (p < 0.001), and LV mass increased from 2.0 +/- 0.3 to 2.6 +/- 0.5 g/kg (p = 0.001). Regionally, the decline in subendocardial %S was greater in adjacent (19 +/- 5% to 8 +/- 5%) than in remote noninfarcted regions (20 +/- 6% to 19 +/- 6%, p < 0.002). No difference in regional blood flow or blood flow reserve was found between adjacent and remote regions, whereas I-123 MIBG uptake was lower in adjacent than in remote myocardium (1.09 +/- 0.30 vs. 1.31 +/- 0.40 nmol/g, p < 0.003). Topographically, from apex to base at 8 weeks after infarction, %S correlated closely with I-123 MIBG uptake (r = 0.93, p = 0.003). CONCLUSIONS: In mechanically dysfunctional noninfarcted regions adjacent to chronic transmural myocardial infarction in the remodeled left ventricle, blood flow and blood flow reserve are preserved, yet sympathetic innervation is reduced. Chronic sympathetic denervation in adjacent noninfarcted regions, in association with regional mechanical dysfunction, may contribute to LV remodeling after infarction.

3-Iodobenzylguanidine↗

Dissociation between changes in intramyocardial function and left ventricular volumes in the eight weeks after first anterior myocardial infarction.

OBJECTIVES: We sought to examine the relation between regional changes in intramyocardial function and global left ventricular (LV) remodeling in the first 8 weeks after reperfused first anterior myocardial infarction (MI). BACKGROUND: Because of limitations in imaging methods used to date, this relation has not been thoroughly evaluated. METHODS: We studied 26 patients (21 men, 5 women; mean age 51 years) by magnetic resonance imaging (MRI) on day 5 +/- 2 (mean +/- SD) and week 8 +/- 1 after their first anterior MI. All patients had single-vessel left anterior descending coronary artery disease and although they had received reperfusion therapy, all had regional LV dysfunction and an initial ejection fraction (EF) < or = 50%. Short-axis magnetic resonance tagging was performed spanning the LV. Percent intramyocardial circumferential shortening (%S) on a topographic basis, LV mass index, LV end-diastolic volume index (LVEDVI), LV end-systolic volume index and LV ejection fraction (LVEF) were measured. RESULTS: Left ventricular mass index tended to decrease, whereas the LVEDVI increased from 82 +/- 24 to 96 +/- 27 ml/m2 (p = 0.002). Left ventricular end-systolic volume index remained unchanged, whereas LVEF increased from 39 +/- 12% to 45 +/- 14% (p = 0.002). Apical %S improved from 9 +/- 6% to 13 +/- 5% (p < 0.0001), as it did in the midanterior (6 +/- 6% to 10 +/- 7%, p < 0.02) and midseptal regions (8 +/- 7% to 12 +/- 6%, p < 0.02). Early dysfunction in remote midinferior and basal lateral regions resolved by 8 weeks. By multivariate analysis, the only significant predictor of an increase in LVEDVI over the study period was peak creatine kinase (p = 0.04). CONCLUSIONS: In the first 8 weeks after a large, reperfused anterior MI, %S improved in the apex, midanterior and midseptal regions and normalized in remote noninfarct-related regions, but LV end-diastolic volumes also increased. This increased LVEDVI correlated with infarct size by peak creatine kinase and was not related to changes in global and regional LV function.

Adult↗

Remote noninfarcted region dysfunction soon after first anterior myocardial infarction. A magnetic resonance tagging study.

BACKGROUND: Previous studies have demonstrated hyperkinetic endocardial motion of noninfarcted myocardium early after myocardial infarction (MI). We wished to substantiate the findings of increased function of remote noninfarcted regions using magnetic resonance (MR) myocardial tagging in patients soon after anterior MI. METHODS AND RESULTS: Twenty-eight patients (25 male; mean age, 52 years) were studied on day 5 +/- 2 after first anterior MI. All had single-vessel left anterior descending coronary artery (LAD) disease and had received reperfusion therapy but had evidence of regional left ventricular (LV) dysfunction and an ejection fraction (EF) < or = 50%. Breath-hold, segmented k-space, gradient-echo MR tagging was performed with short-axis imaging spanning the LV. Percent circumferential shortening (%S) on a topographic basis, LV mass, and EF were measured. Regional %S was compared with that in 10 normal subjects (7 male; mean age, 43 years). We found reduced intramyocardial %S throughout the LV in the patient group. Percent shortening was lower in patients compared with control subjects at all sites along the long axis of the ventricle (9 +/- 5% versus 23 +/- 3% at the apex, P < .0001; 11 +/- 5% versus 21 +/- 3% at the midventricle, P < .0001; 14 +/- 3% versus 17 +/- 5% at the base, P < .02). The basal lateral and midinferior regions, remote from LAD territory, demonstrated reduced %S and a strong trend toward reduced %S, respectively. CONCLUSIONS: Patients on day 5 after first anterior MI with single-vessel disease demonstrate reduced intramyocardial circumferential shortening throughout the LV, including remote noninfarcted regions. Potential mechanisms include altered coronary vasodilatory properties, changes in regional mechanical load, or mechanical tethering to infarcted regions.

Adult↗

Antihypertensive treatment in hypertensive patients with normal left ventricular mass is associated with left ventricular remodeling and improved diastolic function.

Antihypertensive therapy in hypertensive patients with left ventricular (LV) hypertrophy causes hypertrophy regression and improved diastolic filling. Whether similar changes occur in hypertensive patients with diastolic dysfunction and no hypertrophy is unknown. We determined the effect of antihypertensive therapy of LV geometry and function in hypertensive patients without hypertrophy. In 18 mild to moderate hypertensive patients without significant hypertrophy, baseline echocardiograms and rest and exercise and radionuclide angiograms were performed. Subjects were treated for 8 to 12 months with the calcium channel blocker felodipine and then restudied 2 weeks after treatment withdrawal. Blood pressure normalized with treatment (165 +/- 22/98 +/- 9 to 128 +/- 12/80 +/- 5 mm Hg, p <0.001) and returned to pretreatment levels after therapy withdrawal. Rest ejection fraction and peak oxygen consumption and cardiac outputs were unchanged after treatment, but rest peak filling rate increased (2.63 +/- 0.57 to 3.11 +/- 0.95 end-diastolic volume/second, p <0.05). Ejection fraction increased with exercise only after treatment (64 +/- 5% at rest to 71 +/- 8% at peak exercise, p <0.05). LV mass index was unchanged (97 +/- 18 to 101 +/- 23 g/m2), but relative wall thickness declined (0.41 +/- 0.05 to 0.37 +/- 0.05) and LV end-diastolic dimension increased (4.9 +/- 0.4 to 5.2 +/- 0.4, p = 0.01). Blood pressures control in hypertensive patients without hypertrophy leads to improved peak filling rates and remodeling with decreased relative wall thickness. Improved diastolic function can occur without alterations in LV mass.

Antihypertensive Agents↗

Angiotensin-converting enzyme inhibition limits dysfunction in adjacent noninfarcted regions during left ventricular remodeling.

OBJECTIVES: We hypothesized that angiotensin-converting enzyme inhibitors would limit dysfunction in the first 8 weeks after transmural infarction in adjacent noninfarcted regions, as well as attenuate left ventricular remodeling. BACKGROUND: Angiotensin-converting enzyme inhibition limits ventricular dilation and hypertrophy and improves survival after anterior infarction, but its effect on regional function during remodeling is not well characterized. METHODS: Thirteen sheep underwent coronary ligation to create an anteroapical infarction. At postinfarction day 2, eight sheep were randomized to therapy with the angiotensin-converting enzyme inhibitor ramipril, and five sheep received no therapy. Animals were studied with magnetic resonance myocardial tagging before and 8 weeks after infarction. Left ventricular volume, mass and ejection fraction were measured, as were changes in percent circumferential shortening within the subendocardium and subepicardium of infarcted and noninfarcted myocardium, both adjacent to and remote from the infarction. RESULTS: Angiotensin-converting enzyme inhibition limited the increase in end-diastolic volume from a mean (+/- SD) of +1.5 +/- 0.7 ml/kg in control animals to +0.5 +/- 0.8 ml/kg in the treated group (p < 0.04). Segmental function within infarcted and remote noninfarcted tissue did not differ between groups. However, angiotensin-converting enzyme inhibition limited the decline in function in the adjacent noninfarcted region 8 weeks after infarction. Percent circumferential shortening in the subendocardium decreased by -13 +/- 5% in the control group compared with -5 +/- 5% in the treated group (p < 0.03). CONCLUSIONS: In concert with a reduction in left ventricular remodeling after anterior infarction, angiotensin-converting enzyme inhibition limits the decline in function in the adjacent noninfarcted region. Dysfunction in adjacent noninfarcted regions may be an important determinant of left ventricular remodeling after infarction.

Analysis of Variance↗

Left ventricular ejection fraction during supine and upright exercise in patients with systemic hypertension and its relation to peak filling rate.

In hypertensive patients with hypertrophy, abnormal peak filling rate (PFR) is related to a decline in left ventricular (LV) ejection fraction (EF) during supine exercise. Because an increased LV preload is more common during upright exercise, we determined this relation during upright and supine exercise. In 20 hypertensive patients, rest and exercise radionuclide angiography in the supine and upright positions, as well as echocardiography, were performed and compared with 20 age-matched controls. At rest in the supine and upright positions, blood pressure, LVEF, and PFR were 164 +/- 20/94 +/- 10 and 164 +/- 24/94 +/- 10 mm Hg, 65 +/- 8% and 65 +/- 6%, and 2.77 +/- 0.59 and 2.70 +/- 0.52 end-diastolic volumes/s, respectively. PFR was reduced compared with controls (3.29 +/- 0.3 and 3.27 +/- 0.27 end-diastolic volumes/s, supine and upright). LV mass index was normal (94 +/- 19 g/m2). LVEF increased during upright but not during supine exercise in the hypertensives. Four patients had a decline in each position versus none of the controls. There was no relation between the change in LVEF and rest PFR. In patients with mild to moderate hypertension without extensive hypertrophy, abnormal filling rates were present but did not correlate with the change in LVEF with exercise.

Coronary Angiography↗

Segmental motion and deformation of transmurally infarcted myocardium in acute postinfarct period.

Mechanical behavior of infarcted myocardium in the first week following coronary occlusion has not been well characterized. Prior unidimensional studies failed to account for perpendicular deformation or shearing. This study characterizes three-dimensional motion and deformation of transmural infarcts 1 wk after coronary ligation in seven sheep. Principal strains and systolic in-plane translation and rotation were calculated for triangular elements defined by tissue tagging in short- and long-axis magnetic resonance images. The magnitudes of the first and second principal strains were reduced in both the short- and long-axis planes 1 wk after infarction. In addition, the absolute angular difference between the direction of the first principal strain and the radial direction increased from 14.7 +/- 1.9 to 43.5 +/- 2.7 degrees in the short-axis plane and from 19.6 +/- 7.3 to 43.9 +/- 10.0 degrees (P < 0.05) in the long-axis plane. In-plane rigid-body translation and rotation were also reduced in both planes. In conclusion, marked reduction and reorientation of principal strains and reduction in segmental rigid-body motion characterize nonreperfused transmural myocardial infarctions 1 wk after coronary occlusion.

Animals↗

Intracoronary Doppler guide wire versus stress single-photon emission computed tomographic thallium-201 imaging in assessment of intermediate coronary stenoses.

OBJECTIVES: The purpose of this study was to compare measures of coronary flow reserve by an intracoronary Doppler guide wire with results of stress single-photon emission computed tomographic (SPECT) thallium-201 imaging in patients with intermediate coronary artery disease (40% to 70% stenosis). BACKGROUND: Visual assessment of the coronary arteriogram as a means of predicting the physiologic significance of intermediate coronary stenoses is inaccurate. Coronary flow reserve is a reliable marker of the functional importance of a coronary lesion. The recent development of an intracoronary Doppler guide wire permits routine assessment of coronary flow reserve distal to coronary artery stenoses. METHODS: We prospectively evaluated coronary flow reserve in 30 subjects with intermediate stenoses using an intracoronary Doppler guide wire during elective coronary angiography. Patients subsequently underwent stress SPECT thallium-201 testing, and the blinded interpretations were correlated. Coronary flow reserve in a control group with normal coronary arteries classified our sample into group 1 (abnormal flow reserve, < 2.0) and group 2 (normal flow reserve, > or = 2.0). RESULTS: As defined, the coronary flow reserve of 16 vessels in group 1 was diminished in comparison to that of 19 vessels in group 2 (p = 0.0001). Qualitative and quantitative analysis of stress SPECT thallium-201 images confirmed perfusion defects in 15 of 16 vascular territories in group 1 in contrast to 1 of 19 regions in group 2. The sensitivity, specificity and overall predictive accuracy of Doppler-determined coronary flow reserve for stress SPECT thallium-201 results were 94%, 95% and 94%, respectively. CONCLUSIONS: In appropriately selected patients with intermediate coronary artery stenoses, Doppler guide wire determination of lesion significance provides equivalent data to those acquired by stress SPECT thallium-201 imaging.

Aged↗