MRI Measurements of Left Ventricular Systolic Wall Thickening Compared to Regional Myocardial Perfusion as Determined by 201 Tl SPECT in Patients with Coronary Artery Disease

1991 ◽  
Vol 30 (02) ◽  
pp. 61-66 ◽  
Author(s):  
C. Altehoefer ◽  
C. Arnold ◽  
U. Buell ◽  
J. Dahl ◽  
R. Uebis ◽  
...  
Keyword(s):  
Myocardial Perfusion ◽  
Spin Echo ◽  
Posterior Wall ◽  
Anterior Wall ◽  
Left Ventricular ◽  
Wall Thickening ◽  
Myocardial Uptake ◽  
Regional Myocardial Perfusion ◽  
Systolic Wall Thickening ◽  
Mri Measurements

Magnetic resonance imaging (MRI) of the left ventricle (LV) is an excellent method of measuring systolic wall thickening (SWT). The aim of the present study was (a) to describe a new approach for measurement of SWT and (b) to define the relationship between SWT and regional myocardial perfusion as determined by 201TI SPECT. 79 patients - 51 with and 28 without history of earlier myocardial infarction - underwent SPECT and, within the next two weeks, MRI. End-diastolic and end-systolic spin echo images were obtained by a reduced permutation technique. For MRI measurements, only long-axis sections through the LV in the equatorial plane were used. Slice orientation was selected according to the findings of SPECT, imaging the infarcted wall segment by single or double angulation. At 7 equidistant points around the LV wall SWT was measured and compared with the corresponding regional myocardial uptake values from SPECT in percent of maximal perfusion. Wall thickness of the anterior wall was normal. Because the majority of myocardial infarctions were posterior-inferior (55%), thickness of the posterior wall was markedly decreased. A close relationship of perfusion to SWT was found. Higher perfusion areas (>50% of maximal Tl uptake) corresponded with normal SWT (>3.0 mm), a marked decrease of SWT (<1 mm) was found in areas with perfusion deficits (<40%). Thus, a 201TI uptake value at rest of 41-50% of the respective myocardial maximum acts as a threshold by discriminating normal from severely reduced SWT.

Regional myocardial effects of intracoronary bradykinin in conscious dogs

1997 ◽  
Vol 272 (3) ◽  
pp. H1266-H1274 ◽  
Author(s):  
R. Houel ◽  
J. Su ◽  
F. Barbe ◽  
R. Choussat ◽  
B. Crozatier ◽  
...  
Keyword(s):  
Myocardial Function ◽  
Enzyme Inhibitor ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Wall Thickening ◽  
Regional Myocardial Function ◽  
Systemic Hemodynamic ◽  
Systolic Wall Thickening ◽  
Dose Dependent

This study examined in conscious dogs, the coronary and regional myocardial effects of bradykinin (BK) administered by intracoronary route and their modulation by an angiotensin-converting enzyme inhibitor. Eleven dogs were chronically instrumented with a left ventricular (LV) micromanometer, a circumflex coronary catheter, a flow probe, and ultrasonic crystals in the LV posterior wall. In the absence of systemic hemodynamic changes, BK (0.1-10 ng/kg i.c.) produced dose-dependent increases in coronary blood flow velocity (CBFV) and in LV posterior end-diastolic wall thickness (EDWT) but produced no change in LV regional myocardial function as assessed by LV posterior systolic wall thickening. The increases in LV EDWT and CBFV were linearly correlated. The BK B2 antagonist (HOE 140) abolished the effects of BK. Intracoronary enalaprilat (0.75 mg) extended the duration of the effect of BK on CBFV without modification of peak responses and induced a further increase in LV posterior EDWT but no change in LV regional myocardial function. Thus, in conscious dogs, the vasodilator effect of intracoronary BK alone or modulated by enalaprilat is not associated with changes in LV regional myocardial function.

Sympathetic activation induces asynchronous contraction in awake dogs with regional denervation

1988 ◽  
Vol 255 (2) ◽  
pp. H358-H365 ◽  
Author(s):  
D. R. Knight ◽  
Y. T. Shen ◽  
J. X. Thomas ◽  
W. C. Randall ◽  
S. F. Vatner
Keyword(s):  
Adrenergic Receptor ◽  
Posterior Wall ◽  
Receptor Activation ◽  
Anterior Wall ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Wall Thickening ◽  
Neural Activation ◽  
Sympathetic Activation ◽  
Intact Group

To determine effects of regional left ventricular (LV) denervation on regional contractile responses to sympathetic activation, dogs with posterior LV wall denervation (posterior wall-denervated group) and dogs with innervated posterior LV walls (intact group) were studied during excitement, exercise, bilateral sympathetic nerve stimulation, and norepinephrine infusion. In intact conscious dogs, all modes of sympathetic activation increased the magnitude and decreased the time of onset of systolic wall thickening (WT) similarly in the anterior and posterior wall. In the denervated group, excitement failed to increase posterior WT during systole but instead elicited asynchronous contraction, i.e., postsystolic WT, as well as delayed onset of contraction. Asynchronous contraction was not observed with excitement after beta-adrenergic receptor blockade. Asynchronous contraction of the posterior wall was also observed during the initial phase of exercise in conscious dogs and during bilateral stellate stimulation in anesthetized dogs in the posterior wall-denervated group. In comparison to neural activation, adrenergic receptor activation with norepinephrine (0.2 microgram/kg-1.min-1 iv) induced a supersensitive increase in systolic WT in the denervated posterior wall (36 +/- 5%) compared with the anterior wall (17 +/- 2%) and a delay in the end of contraction in the anterior region. Thus asynchronous contraction can be elicited in dogs with regional LV denervation as a result of an early and enhanced contraction in the innervated region during neural sympathetic activation. The reverse was observed with systemic administration of norepinephrine because of catecholamine supersensitivity in the denervated posterior wall.

Assessment of Myocardial Viability in Persistent Defects on Thallium-201 SPECT after Reinjection Using Gradient-Echo MRI

1996 ◽  
Vol 35 (05) ◽  
pp. 146-152 ◽  
Author(s):  
A. Kögler ◽  
H.-A. Schmitt ◽  
D. Emrich ◽  
H. Kreuzer ◽  
D. L. Munz ◽  
...  
Keyword(s):  
Wall Thickness ◽  
Myocardial Viability ◽  
Cardiac Cycle ◽  
Single Photon ◽  
Contractile Function ◽  
Left Ventricular ◽  
Wall Thickening ◽  
Gradient Echo ◽  
Systolic Wall Thickening

SummaryThis prospective study assessed myocardial viability in 30 patients with coronary heart disease and persistent defects despite reinjection on TI-201 single-photon computed tomography (SPECT). In each patient, three observers graded TI-201 uptake in 7 left ventricular wall segments. Gradient-echo magnetic resonance imaging in the region of the persistent defect generated 12 to 16 short axis views representing a cardiac cycle. A total of 120 segments were analyzed. Mean end-diastolic wall thickness and systolic wall thickening (± SD) was 11.5 ± 2.7 mm and 5.8 ± 3.9 mm in 48 segments with normal TI-201 uptake, 10.1 ± 3.4 mm and 3.7 ± 3.1 mm in 31 with reversible lesions, 11.3 ± 2.8 mm and 3.3 ± 1.9 mm in 10 with mild persistent defects, 9.2 ± 2.9 mm and 3.2 ±2.2 mm in 15 with moderate persistent defects, 5.8 ± 1.7 mm and 1.3 ± 1.4 mm in 16 with severe persistent defects, respectively. Significant differences in mean end-diastolic wall thickness (p <0.0005) and systolic wall thickening (p <0.005) were found only between segments with severe persistent defects and all other groups, but not among the other groups. On follow-up in 11 patients after revascularization, 6 segments with mild-to-moderate persistent defects showed improvement in mean systolic wall thickening that was not seen in 6 other segments with severe persistent defects. These data indicate that most myocardial segments with mild and moderate persistent TI-201 defects after reinjection still contain viable tissue. Segments with severe persistent defects, however, represent predominantly nonviable myocardium without contractile function.

scholarly journals Effects of Long-term Nonylphenol Exposure on Myocardial Fibrosis and Cardiac Function in Rats

2021 ◽  
Author(s):  
Chao Liu ◽  
Chengyu Ni ◽  
Weichu Liu ◽  
Xiaolian Yang ◽  
Renyi Zhang ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Myocardial Fibrosis ◽  
Posterior Wall ◽  
Anterior Wall ◽  
Left Ventricular ◽  
Environmental Estrogens ◽  
Control Group ◽  
Cardiac Structure ◽  
Collagen Iii

Abstract Background: Myocardial fibrosis is a critical pathological basis for the poor prognosis of cardiovascular diseases. Studies have found that myocardial fibrosis is closely associated with exposure to environmental estrogens such as nonylphenol (NP), as a representative of environmental estrogens. The aim of this study was to examine the effects of NP chronic exposure on myocardial fibrosis as well as cardiac structure and function. Forty Sprague Dawley rats were randomly divided into four groups (n = 10): control group (C), low NP dose (0.4 mg/kg, L), medium NP dose (4 mg/kg, M), and high NP dose (40 mg/kg, H) groups. The NP dose groups were gavaged with NP for 180 days. Results: The NP level in the heart of the NP groups was significantly higher than those in the control group (F = 43.658, P < 0.001). Serum aspartate aminotransferase (AST), creatine kinase (CK), creatine kinase isozyme (CK-MB), lactate dehydrogenase (LDH) and α-hydroxybutyrate dehydrogenase (α-HBDH) significantly increased in the NP groups compared with the control group (). Histopathological examination of the heart biopsy illustrates that in the medium and high NP groups, the fibrous connective tissue had a disordered and loose gridding shape, muscle fibers had fractured, and muscle fibers were loose with a widened gap. Extensive inflammatory cell infiltration and fibroblast proliferation in the myocardial interstitium were also found. With increasing NP dose, the degree of muscle fiber loosing and disorder became more significant in the NP treatment groups, and the collagen volume fraction (CVF) was higher than that in the control group (P < 0.01). Compared with the control group, the expression of collagen I and collagen III increased significantly in the medium and high NP groups (P < 0.05). The values of the systolic thickness of the left ventricular anterior wall (LVAWs), the diastolic thickness of the left ventricular posterior wall (LVPWd), the systolic thickness of the left ventricular posterior wall (LVPWs), and the left ventricular anterior wall (LVAWd) in the NP groups are were slightly lower than those in of the control group. The values of left ventricular end systolic dimensions (LVIDs) in the NP groups increased compared with the control group. Conclusions: Long-term NP exposure could lead to fibrosis in the rat myocardium, which is characterized by increased expressions of myocardial collagen I and collagen III, as well as elevated cardiac enzymes. In addition, the cardiac structure was affected and changes were observed in the thinner ventricular wall and as an enlarged ventricular cavity.

Placental growth factor increases regional myocardial blood flow and contractile function in chronic myocardial ischemia

2013 ◽  
Vol 304 (6) ◽  
pp. H885-H894 ◽  
Author(s):  
Xiaoshun Liu ◽  
Piet Claus ◽  
Ming Wu ◽  
Geert Reyns ◽  
Peter Verhamme ◽  
...  
Keyword(s):  
Blood Flow ◽  
Growth Factor ◽  
Myocardial Perfusion ◽  
Contractile Function ◽  
Placental Growth Factor ◽  
Regional Myocardial Blood Flow ◽  
Wall Thickening ◽  
Systolic Wall Thickening ◽  
Regional Myocardial Blood ◽  
Chronic Myocardial Ischemia

Placental growth factor (PlGF) has a distinct biological phenotype with a predominant proangiogenic role in disease without affecting quiescent vessels in healthy organs. We tested whether systemic administration of recombinant human (rh)PlGF improves regional myocardial blood flow (MBF) and systolic function recovery in a porcine chronic myocardial ischemia model. We implanted a flow-limiting stent in the proximal left anterior descending coronary artery and measured systemic hemodynamics, regional myocardial function using MRI, and blood flow using colored microspheres 4 wk later. Animals were then randomized in a blinded way to receive an infusion of rhPlGF (15 μg·kg−1·day−1, n = 9) or PBS (control; n = 10) for 2 wk. At 8 wk, myocardial perfusion and function were reassessed. Infusion of rhPlGF transiently increased PlGF serum levels >30-fold (1,153 ± 180 vs. 33 ± 18 pg/ml at baseline, P < 0.001) without affecting systemic hemodynamics. From 4 to 8 wk, rhPlGF increased regional MBF from 0.46 ± 0.11 to 0.85 ± 0.16 ml·min−1·g−1, with a concomitant increase in systolic wall thickening from 11 ± 3% to 26 ± 5% in the ischemic area. In control animals, no significant changes from 4 to 8 wk were observed (MBF: 0.45 ± 0.07 to 0.49 ± 0.08 ml·min−1·g−1 and systolic wall thickening: 14 ± 4% to 18 ± 1%). rhPlGF-induced functional improvement was accompanied by increased myocardial neovascularization, enhanced glycogen utilization, and reduced oxidative stress and cardiomyocyte apoptosis in the ischemic zone. In conclusion, systemic rhPlGF infusion significantly enhances regional blood flow and contractile function of the chronic ischemic myocardium without adverse effects. PlGF protein infusion may represent an attractive therapeutic strategy to increase myocardial perfusion and energetics in chronic ischemic cardiomyopathy.

Coronary hyperperfusion augments myocardial oxygen consumption

1996 ◽  
Vol 271 (4) ◽  
pp. H1384-H1393 ◽  
Author(s):  
Y. Ishibashi ◽  
J. Zhang ◽  
D. J. Duncker ◽  
C. Klassen ◽  
T. Pavek ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Myocardial Oxygen Consumption ◽  
Contractile Function ◽  
Left Ventricular ◽  
Wall Thickening ◽  
Systolic Thickening ◽  
Subepicardial Layer ◽  
Systolic Wall Thickening

This study was performed to test the hypothesis that increases in myocardial oxygen consumption (MVo2) and myocardial contractile function during exercise are flow limited. Studies were performed in 15 chronically instrumented normal dogs. MVo2 and regional percent systolic wall thickening were measured during control conditions and during maximal vasodilation produced by infusion of adenosine (20-75 micrograms.kg-1.min-1) or adenosine combined with nitroglycerin (0.4 micrograms.kg-1.min-1; TNG) into the left anterior descending coronary artery during a three-stage graded treadmill exercise protocol. Adenosine and adenosine plus TNG significantly increased coronary blood flow by 298 +/- 26 and 306 +/- 24%, respectively, at rest and by 134 +/- 7 and 145 +/- 9%, respectively, during the heaviest level of exercise (each P < 0.01). Adenosine and adenosine plus TNG increased MVo2 at rest, but this was associated with a parallel increase in heart rate, so that MVo2 per beat was not significantly changed. Systolic wall thickening was also not changed by hyperperfusion during resting conditions. However, MVo2 per beat was increased by 12 +/- 4% with adenosine and by 13 +/- 5% with adenosine plus TNG during moderate exercise and by 23 +/- 5% with adenosine and by 27 +/- 4% with adenosine plus TNG during the heaviest level of exercise (each P < 0.05). Systolic thickening of the full left ventricular wall did not change during hyperperfusion, but thickening in the subepicardial layer was increased by 14 +/- 3% with adenosine and 18 +/- 3% with adenosine plus TNG during the heaviest level of exercise (each P < 0.05). There was no difference in wall thickening between adenosine and adenosine plus TNG. These findings imply that the increases in MVo2 which occur during exercise are limited by coronary blood flow.

Progressive cardiac dysfunction with repeated pacing-induced ischemia: protection by AICA-riboside

1991 ◽  
Vol 261 (5) ◽  
pp. H1570-H1577 ◽  
Author(s):  
M. A. Young ◽  
K. M. Mullane
Keyword(s):  
Blood Flow ◽  
Regional Wall Motion ◽  
Posterior Wall ◽  
Saline Group ◽  
Left Ventricular ◽  
Saline Control ◽  
Regional Myocardial Blood Flow ◽  
Control Group ◽  
Wall Thickening ◽  
Progressive Decline

The effects of repeated episodes of demand-induced ischemia on regional myocardial wall thickening, endocardial electrogram, and regional myocardial blood flow are not well delineated. We studied the cumulative effects of six periods of pacing-induced ischemia in 35 chloralose-anesthetized dogs with circumflex coronary stenosis. Repetitive ischemia of the posterior left ventricular free wall was induced with six 5-min pacing periods separated by 15-min recovery periods. The three groups of dogs studied were 1) saline control, 2) the purine precursor 5-aminoimidazole 4-carboxamide riboside (AICA-r), and 3) nitroglycerin (NTG). During the initial pacing period (before treatment), thickening of the posterior wall declined in the saline group (43 +/- 5% of control), the AICA-r group (47 +/- 8% of control), and the NTG group (55 +/- 3% of control), associated with endocardial S-T segment elevation and a decrease in subendocardial blood flow. Wall thickening continued to decrease in each group with each successive pacing episode. However, during the sixth pacing period wall thickening was significantly (P less than 0.05) less in the saline group (2 +/- 5% of control) than in the AICA-r (31 +/- 7% of control) or NTG (61 +/- 7% of control) group. The progressive decline in wall thickening was accompanied by a further decrease in subendocardial blood flow and a rise in S-T segment in the saline group but not in the AICA-r or NTG group (P less than 0.05). These results demonstrate that sequential periods of ischemia and reperfusion cause a progressive decline in regional wall motion, coincident with a progressive decrease in subendocardial blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Nonuniform transmural recovery of contractile function in stunned myocardium

1989 ◽  
Vol 257 (2) ◽  
pp. H375-H385 ◽  
Author(s):  
R. Bolli ◽  
B. S. Patel ◽  
C. J. Hartley ◽  
J. I. Thornby ◽  
M. O. Jeroudi ◽  
...  
Keyword(s):  
Contractile Function ◽  
Recovery Of Function ◽  
Left Ventricular ◽  
Stunned Myocardium ◽  
Wall Thickening ◽  
Base Line ◽  
Doppler Probe ◽  
Group 2 ◽  
Systolic Wall Thickening ◽  
Group 1

With the use of an epicardial Doppler probe, systolic wall thickening was selectively measured in the inner, mid, and outer layers of the left ventricular (LV) wall in 16 conscious dogs undergoing a 15-min left anterior descending artery (LAD) occlusion followed by 7 days of reperfusion (REP). Under control conditions, percent thickening fraction (ThF) was significantly greater (P less than 0.01) in the inner layer [36.0 +/- 2.3% (mean +/- SE)] than in the mid (28.6 +/- 2.1%) or outer (21.3 +/- 2.2%) layers. During LAD occlusion, 11 dogs exhibited transmural dyskinesis (group 1), whereas 5 had transmural hypokinesis (group 2). In group 1, all layers exhibited comparable degrees of paradoxical systolic thinning during LAD occlusion. After REP, however, recovery was delayed in the inner compared with the mid and outer layers. At 2 h, ThF averaged 34.2 +/- 11.9% of base line in the endocardium vs. 61.7 +/- 16.2% in the midmyocardium and 51.0 +/- 12.3% in the epicardium (F = 4.29, P less than 0.002); similar differences were noted at 3 and 4 h. In the mid and outer layers, ThF returned to base-line values by 24 h, whereas in the inner layer it was still significantly depressed (P less than 0.05) at 24 h (77.3 +/- 5.1% of base line) and recovered by 48 h. The inner-to-outer ThF ratio was decreased (P less than 0.01) for 24 h after REP, indicating maldistribution of thickening in the "stunned" myocardium. In group 2, all layers exhibited hypokinesis during LAD occlusion. Again, recovery of function after REP was delayed in the endocardium compared with the other layers. This study demonstrates that after both severe ischemia resulting in dyskinesis and mild ischemia resulting in hypokinesis, REP is associated with slower recovery of function in the inner than in the outer layers. Thus myocardial "stunning" is a nonuniform phenomenon with maximal severity in the subendocardium.

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