Effect of nitroglycerin and ibuprofen on left ventricular topography and rupture threshold during healing after myocardial infarction in the dog

1988 ◽  
Vol 66 (4) ◽  
pp. 385-395 ◽  
Author(s):  
Bodh I. Jugdutt
Keyword(s):  
Systolic Function ◽  
Left Ventricular ◽  
Mechanical Resistance ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Cross Sectional ◽  
Balloon Technique ◽  
Dimensional Echocardiography ◽  
Improved Function ◽  
And Function

The effect of nitroglycerin and ibuprofen, given between 2 and 7 days after left anterior descending coronary artery ligation, on the mechanical resistance of the infarcted left ventricle to rupture or the rupture threshold (balloon technique), and on topography (computerized planimetry) and function (two-dimensional echocardiography) at 7 days (n = 32) and 42 days (n = 34) postligation was studied in 66 dogs randomly allocated to sham (no infarction, n = 22) and infarction subgroups (15 controls; 15 received nitroglycerin, 30 mg oral isosorbide dinitrate b.i.d; 14 received ibuprofen, 200 mg t.i.d orally). Nitroglycerin decreased mean arterial and left atrial pressures, decreased diastolic cross-sectional area, and improved systolic function, while ibuprofen increased diastolic area. Infarction subgroups showed infarct shrinkage and more infarct hydroxyproline at 6 weeks. Compared with shams, all infarct subgroups showed early expansion and thinning, with further marked late thinning in controls. Nitroglycerin produced less expansion and thinning both at 1 and 6 weeks, while ibuprofen produced marked early thinning. Rupture threshold was less at 6 weeks than 1 week with controls and ibuprofen but remained unchanged with nitroglycerin. Passive prerupture stiffness was less at 6 weeks than at 1 week in controls but remained unchanged with nitroglycerin and ibuprofen. Thus, reduced expansion and thinning with nitroglycerin during the first week after infarction improved function, mechanical strength, and resistance to distension at 6 weeks.

scholarly journals Progression of heart failure after myocardial infarction in the rat

2001 ◽  
Vol 281 (5) ◽  
pp. R1734-R1745 ◽  
Author(s):  
J. Francis ◽  
R. M. Weiss ◽  
S. G. Wei ◽  
A. K. Johnson ◽  
R. B. Felder
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Ventricular Remodeling ◽  
Systolic Function ◽  
Left Ventricular Remodeling ◽  
Plasma Renin ◽  
Left Ventricular Systolic Function ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation

This study examined the early neurohumoral events in the progression of congestive heart failure (CHF) after myocardial infarction (MI) in rats. Immediately after MI was induced by coronary artery ligation, rats had severely depressed left ventricular systolic function and increased left ventricular end-diastolic volume (LVEDV). Both left ventricular function and the neurohumoral indicators of CHF underwent dynamic changes over the next 6 wk. LVEDV increased continuously over the study interval, whereas left ventricular stroke volume increased but reached a plateau at 4 wk. Plasma renin activity (PRA), arginine vasopressin, and atrial natriuretic factor all increased, but with differing time courses. PRA declined to a lower steady-state level by 4 wk. Six to 8 wk after MI, CHF rats had enhanced renal sympathetic nerve activity and blunted baroreflex regulation. These findings demonstrate that the early course of heart failure is characterized not by a simple “switching on” of neurohumoral drive, but rather by dynamic fluctuations in neurohumoral regulation that are linked to the process of left ventricular remodeling.

Abstract P229: Chymase-mediated Igf-1 Degradation Promotes Delayed Cell Death in Post-ischemic Hearts

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Lin Tan ◽  
Thor Tejada ◽  
Rebecca Torres ◽  
John Calvert ◽  
Gunnar Pejler ◽  
...  
Keyword(s):  
Heart Disease ◽  
Systolic Function ◽  
Left Ventricular Systolic Function ◽  
Left Ventricular ◽  
P Value ◽  
Coronary Artery Ligation ◽  
Ventricular Systolic Function ◽  
Artery Ligation ◽  
Delayed Cell Death ◽  
Mouse Mast Cell

Heart disease is a leading cause of death in adults. Here we show that a few days after coronary artery ligation and reperfusion, the ischemia-injured heart elaborates the cardioprotective polypeptide, insulin-like growth factor-1 (IGF-1), which activates IGF-1 receptor prosurvival signaling and improves cardiac left ventricular systolic function. However, this is antagonized by the chymase, mouse mast cell protease-4 (MMCP-4), which degrades IGF-1 (Fig. 1). We found that MMCP-4 deficiency, resulted in sustained IGF-1 levels and IGF-1 receptor prosurvival signaling post-I/R. MMCP-4 deficiency markedly reduced late, but not early, infarct size (~50% reduction: n=5-7, p value= 0.001) by suppressing IGF-1 degradation and, consequently, improving cardiac function (EF: 26% greater, n=21, p value= 0.001) and adverse structural remodeling (Fig. 2). Our findings represent the first demonstration of tissue IGF-1 regulation through proteolytic degradation and suggest that chymase inhibition may be a viable therapeutic approach to enhance late cardioprotection in post-ischemic heart disease.

Cardiovascular adaptations to 10 days of cycle exercise

1997 ◽  
Vol 83 (6) ◽  
pp. 1900-1906 ◽  
Author(s):  
Constance M. Mier ◽  
Michael J. Turner ◽  
Ali A. Ehsani ◽  
Robert J. Spina
Keyword(s):  
Systolic Function ◽  
Wall Stress ◽  
Cycle Ergometer ◽  
Left Ventricular ◽  
Peak Exercise ◽  
Inotropic Response ◽  
Adrenergic Stimulation ◽  
Cycle Exercise ◽  
Dimensional Echocardiography ◽  
And Function

Mier, Constance M., Michael J. Turner, Ali A. Ehsani, and Robert J. Spina. Cardiovascular adaptations to 10 days of cycle exercise. J. Appl. Physiol. 83(6): 1900–1906, 1997.—We hypothesized that 10 days of training would enhance cardiac output (CO) and stroke volume (SV) during peak exercise and increase the inotropic response to β-adrenergic stimulation. Ten subjects [age 26 ± 2 (SE) yr] trained on a cycle ergometer for 10 days. At peak exercise, training increased O2 uptake, CO, and SV ( P < 0.001). Left ventricular (LV) size and function at rest were assessed with two-dimensional echocardiography before (baseline) and after atropine injection (1.0 mg) and during four graded doses of dobutamine. LV end-diastolic diameter increased with training ( P< 0.02), whereas LV wall thickness was unchanged. LV contractile performance was assessed by relating fractional shortening (FS) to the estimated end-systolic wall stress (ςES). Training increased the slope of the FS-ςES relationship ( P < 0.05), indicating enhanced systolic function. The increase in slope correlated with increases in CO ( r = −0.71, P < 0.05) and SV ( r = −0.70, P < 0.05). The increase in blood volume also correlated with increases in CO ( r = 0.80, P < 0.01) and SV ( r= 0.85, P < 0.004). These data show that 10 days of training enhance the inotropic response to β-adrenergic stimulation, associated with increases in CO and SV during peak exercise.

scholarly journals Left atrial structure and function among different subtypes of atrial fibrillation: an echocardiographic substudy of the AMIO-CAT trial

2020 ◽  
Vol 21 (12) ◽  
pp. 1386-1394
Author(s):  
Flemming Javier Olsen ◽  
Stine Darkner ◽  
Xu Chen ◽  
Steen Pehrson ◽  
Arne Johannessen ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Left Atrial ◽  
Systolic Function ◽  
Holter Monitoring ◽  
Left Ventricular ◽  
Structure And Function ◽  
Cross Sectional ◽  
Cardiac Structure And Function ◽  
And Function ◽  
Study Inclusion

Abstract Aims  Little is known about cardiac structure and function among atrial fibrillation (AF) subtypes; paroxysmal AF vs. persistent AF (PxAF), and across AF burden. We sought to assess differences in left atrial (LA) measures by AF subtype and burden. Methods and results  This was a cross-sectional echocardiographic substudy of a randomized trial of AF patients scheduled for catheter ablation. Patients had an echocardiogram performed 0–90 days prior to study inclusion. We performed conventional echocardiographic measures, left ventricular (LV) and LA speckle tracking. Measures were compared between AF subtype and burden (0%, 0–99%, and 99–100%) determined by 72-h Holter monitoring. Of 212 patients, 107 had paroxysmal AF and 105 had PxAF. Those with PxAF had significantly reduced systolic function (LV ejection fraction: 48% vs. 53%; P &lt; 0.001), larger end-systolic and end-diastolic LA volumes (LAVi and LAEDVi), reduced LA emptying fraction (LAEF: 29% vs. 36%, P &lt; 0.001), and reduced LA strain (LAs) (LAs: 20% vs. 26%, P &lt; 0.001). LA measures remained significantly lower in PxAF after multivariable adjustments. All LA measures and measures of systolic function were significantly impaired in patients with 99–100% AF burden, whereas all measures were similar between the other groups (LAVi: 40mL/m2 vs. 33mL/m2 vs. 34mL/m2; LAEDVi: 31mL/m2 vs. 21mL/m2 vs. 22mL/m2, LA emptying fraction: 23% vs. 35% vs. 36%, LAs: 16% vs. 25% vs. 25%, for 99–100%, 0–99%, and 0% AF, respectively, P &lt; 0.001 for all). These differences were consistent after multivariable adjustments. Conclusion  LA mechanics differ between AF subtype and burden and these characteristics influence the clinical interpretation of these measures.

scholarly journals IGF-1 degradation by mouse mast cell protease 4 promotes cell death and adverse cardiac remodeling days after a myocardial infarction

2016 ◽  
Vol 113 (25) ◽  
pp. 6949-6954 ◽  
Author(s):  
Thor Tejada ◽  
Lin Tan ◽  
Rebecca A. Torres ◽  
John W. Calvert ◽  
Jonathan P. Lambert ◽  
...  
Keyword(s):  
Mast Cell ◽  
Heart Disease ◽  
Systolic Function ◽  
Left Ventricular Systolic Function ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Gene Encoding ◽  
Artery Ligation ◽  
Mast Cell Protease ◽  
Mouse Mast Cell

Heart disease is a leading cause of death in adults. Here, we show that a few days after coronary artery ligation and reperfusion, the ischemia-injured heart elaborates the cardioprotective polypeptide, insulin-like growth factor-1 (IGF-1), which activates IGF-1 receptor prosurvival signaling and improves cardiac left ventricular systolic function. However, this signaling is antagonized by the chymase, mouse mast cell protease 4 (MMCP-4), which degrades IGF-1. We found that deletion of the gene encoding MMCP-4 (Mcpt4), markedly reduced late, but not early, infarct size by suppressing IGF-1 degradation and, consequently, diminished cardiac dysfunction and adverse structural remodeling. Our findings represent the first demonstration to our knowledge of tissue IGF-1 regulation through proteolytic degradation and suggest that chymase inhibition may be a viable therapeutic approach to enhance late cardioprotection in postischemic heart disease.

Echocardiographic evaluation of size, function, and mass of normal and hypertrophied rat ventricles

1993 ◽  
Vol 74 (5) ◽  
pp. 2598-2605 ◽  
Author(s):  
D. G. Pawlush ◽  
R. L. Moore ◽  
T. I. Musch ◽  
W. R. Davidson
Keyword(s):  
Systolic Function ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Structure And Function ◽  
Cardiac Structure ◽  
Echocardiographic Evaluation ◽  
Mechanical Transducer ◽  
Cardiac Structure And Function ◽  
Dimensional Echocardiography ◽  
And Function

The noninvasive evaluation of cardiac structure and function in small animals would provide a means for investigators to repeatedly evaluate treatment effects at various stages of experimental protocols. In this study, commercially available echocardiographic and Doppler equipment was utilized to evaluate hypertrophied (HYP) and normal (SH) rat hearts. Surgically induced renovascular hypertension was used to produce a 35% increase in left ventricular (LV) weight in HYP relative to SH hearts. A commercially available echocardiographic system with integral Doppler capabilities and a 7.5-mHz single-crystal mechanical transducer was used to obtain parasternal long- and short-axis images of HYP and SH hearts in anesthetized animals. HYP hearts were found to have normal systolic function, as evidenced by preserved LV systolic and diastolic dimensions and volumes as well as fractional shortening and ejection fraction. HYP hearts demonstrated a 62% increase in their echocardiographically measured LV posterior wall thicknesses and a 44% increase in calculated ventricular mass. Both parameters were reliable in predicting the presence and degree of left ventricular hypertrophy. Doppler flow velocities through the aortic root and pulmonic valve did not differ between groups, again suggesting preserved LV systolic performance. These results indicate that two-dimensional echocardiography provides a useful means to noninvasively evaluate cardiac structure and function in rats.

Left ventricular rupture threshold during the healing phase after myocardial infarction in the dog

1987 ◽  
Vol 65 (3) ◽  
pp. 307-316 ◽  
Author(s):  
Bodh I. Jugdutt
Keyword(s):  
Left Ventricle ◽  
Dry Weight ◽  
Left Ventricular ◽  
Mechanical Resistance ◽  
Coronary Artery Ligation ◽  
Infarct Zone ◽  
Artery Ligation ◽  
Average Value ◽  
Left Ventricular Stiffness ◽  
Healing Phase

The mechanical resistance of the infarcted left ventricle to rupture, or rupture threshold, was measured by the balloon technique 1–42 days after left anterior descending coronary artery ligation in 70 dogs: 26 without infarction (18 sham, 8 with ligation) and 44 with infarction. Rupture threshold in noninfarcted hearts was higher than in infarcted hearts (1168 ± 165 (SD) vs. 754 ± 223 mmHg (1 mmHg = 133.32 Pa), p < 0.001) and did not change over 6 weeks. In contrast, rupture threshold in infarcted hearts decreased (p < 0.05) after 14 days, the average value for 21–42 days being less than that for 1–14 days: 577 ± 140 vs. 867 ± 191 mmHg, p < 0.001. Passive left ventricular stiffness in infarcted hearts was higher than for noninfarcted hearts throughout the 6 weeks during early filling (11.1 ± 3.9 vs. 7.1 ± 1.4 mmHg/mL, p < 0.001) but decreased (p < 0.05) after 14 days during the prerupture phase (11.3 ± 5.3 vs. 6.2 ± 3.0 mmHg/mL, p < 0.005). Between 7 and 42 days, the infarct zone showed marked increase in hydroxyproline (10.0 ± 2.0 vs. 48.8 ± 19.7 mg/g dry weight, p < 0.001), shrinkage (infarct size, 25 ± 9 vs. 9 ± 5% of the left ventricle, p < 0.005), and thinning (infarct to normal wall thickness ratio, 0.83 ± 0.11 vs. 0.51 ± 0.09, p < 0.001) but little further stretching (expansion index or the ratio of lengths of infarcted and noninfarcted segments, 1.14 ± 0.10 vs. 1.28 ± 0.17, p < 0.2). A mild decrease (p < 0.05) in left atrial pressure and increase (p < 0.05) in diastolic area and fractional change in area (two-dimensional echocardiography) were detected at 6 weeks. The late decrease in rupture threshold and prerupture stiffness of the infarcted left ventricle and thinning of the scar suggest a late decrease in mechanical strength and resistance of the infarcted left ventricle to distension.

Effects of avertin versus xylazine-ketamine anesthesia on cardiac function in normal mice

2001 ◽  
Vol 281 (5) ◽  
pp. H1938-H1945 ◽  
Author(s):  
Chari Y. T. Hart ◽  
John C. Burnett ◽  
Margaret M. Redfield
Keyword(s):  
Cardiac Function ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Lv Function ◽  
Ketamine Anesthesia ◽  
The Difference ◽  
And Function ◽  
Derivatives Of

Anesthetic regimens commonly administered during studies that assess cardiac structure and function in mice are xylazine-ketamine (XK) and avertin (AV). While it is known that XK anesthesia produces more bradycardia in the mouse, the effects of XK and AV on cardiac function have not been compared. We anesthetized normal adult male Swiss Webster mice with XK or AV. Transthoracic echocardiography and closed-chest cardiac catheterization were performed to assess heart rate (HR), left ventricular (LV) dimensions at end diastole and end systole (LVDd and LVDs, respectively), fractional shortening (FS), LV end-diastolic pressure (LVEDP), the time constant of isovolumic relaxation (τ), and the first derivatives of LV pressure rise and fall (dP/d t max and dP/d t min, respectively). During echocardiography, HR was lower in XK than AV mice (250 ± 14 beats/min in XK vs. 453 ± 24 beats/min in AV, P < 0.05). Preload was increased in XK mice (LVDd: 4.1 ± 0.08 mm in XK vs. 3.8 ± 0.09 mm in AV, P < 0.05). FS, a load-dependent index of systolic function, was increased in XK mice (45 ± 1.2% in XK vs. 40 ± 0.8% in AV, P < 0.05). At LV catheterization, the difference in HR with AV (453 ± 24 beats/min) and XK (342 ± 30 beats/min, P < 0.05) anesthesia was more variable, and no significant differences in systolic or diastolic function were seen in the group as a whole. However, in XK mice with HR <300 beats/min, LVEDP was increased (28 ± 5 vs. 6.2 ± 2 mmHg in mice with HR >300 beats/min, P < 0.05), whereas systolic (LV dP/d t max: 4,402 ± 798 vs. 8,250 ± 415 mmHg/s in mice with HR >300 beats/min, P < 0.05) and diastolic (τ: 23 ± 2 vs. 14 ± 1 ms in mice with HR >300 beats/min, P < 0.05) function were impaired. Compared with AV, XK produces profound bradycardia with effects on loading conditions and ventricular function. The disparate findings at echocardiography and LV catheterization underscore the importance of comprehensive assessment of LV function in the mouse.

Abstract 402: Vitamin C Deficiency Impairs Cardiac Function and Post-infarction Survival in the Mouse

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Adolfo G Mauro ◽  
Donatas Kraskauskas ◽  
Bassem M Mohammed ◽  
Bernard J Fisher ◽  
Eleonora Mezzaroma ◽  
...  
Keyword(s):  
Vitamin C ◽  
Cardiac Function ◽  
Diastolic Function ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Additional Group ◽  
Gulonolactone Oxidase ◽  
Low Levels ◽  
Systolic And Diastolic Function

Introduction: L-gulonolactone oxidase (Gulo) is the rate limiting enzyme for Vitamin C (VitC) biosynthesis. Humans rely on dietary VitC for collagen synthesis, extracellular matrix formation, and tissue regeneration. VitC deficiency is an unrecognized condition and its role in cardiac homeostasis and post-acute myocardial infarction (AMI) remodeling is unknown. Hypothesis: Low levels of VitC impair cardiac function and tissue repair following AMI. Methods: Adult male Gulo -/- knockout mice (C57BL6 background, N=8) and control C57BL (N=8), which are able to synthesize VitC were used. VitC deficiency was maintained supplying low levels of VitC (30mg/l) to Gulo -/- mice in drinking water. Mice underwent M-mode and Doppler echocardiography to measure left ventricular (LV) diameters and wall thicknesses, fractional shortening (FS), E and A waves, E/A ratio, isovolumetric relaxation time (IRT) and myocardial performance index (MPI). Experimental AMI was induced by coronary artery ligation for 7 days. An additional group of Gulo -/- were mice supplemented with physiological levels of VitC (330 mg/l) and underwent AMI. Results: VitC deficient Gulo -/- mice exhibited significantly reduced LV wall thicknesses, reduced FS, and impaired diastolic function, measured as significantly reduced E/A ratio and longer IRT (Panel A, B & C). Following AMI, 100% (8/8) of deficient Gulo -/- mice died within 5 days. Supplementation with physiological levels of VitC significantly improved survival after AMI (Panel D). Conclusion: VitC deficiency impairs systolic and diastolic function. Moreover, VitC is critical for the post-AMI survival.

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