Effects of arterial hypertension on myocardial recovery after ischemic injury

1992 ◽  
Vol 263 (2) ◽  
pp. H559-H564 ◽  
Author(s):  
J. R. Elbeery ◽  
R. F. Williams ◽  
J. S. Rankin ◽  
D. D. Glower ◽  
D. C. Sabiston ◽  
...  
Keyword(s):  
Arterial Hypertension ◽  
Systolic Function ◽  
Ischemic Injury ◽  
Left Ventricular ◽  
Segment Length ◽  
Myocardial Segment ◽  
Stroke Work ◽  
Myocardial Recovery ◽  
Length Relationship ◽  
Injured Myocardium

Although improved surgery, angioplasty, and thrombolysis have made early revascularization of ischemic myocardium commonplace, the effects of arterial hypertension on myocardial recovery remain unclear. Therefore eight conscious dogs were instrumented to measure left ventricular transmural pressure and myocardial segment length in the left anterior descending (LAD) coronary distribution. Reversible ischemic injury was produced by two 15-min LAD occlusions separated by 4 days of reperfusion, with each dog randomly receiving either phenylephrine or placebo infusion for 30 min beginning 1 h after reperfusion. With ischemia, systolic myocardial performance fell to 14.3 +/- 3.7% of control and required greater than 48 h to recover. Compared with placebo, phenylephrine significantly depressed recovery of systolic function assessed by systolic shortening (57 +/- 12 vs. 85 +/- 13% control) or the area under the stroke work vs. end-diastolic length relationship (62 +/- 14 vs. 93 +/- 7% control) (both P less than 0.05). These data imply that ischemically injured myocardium is highly sensitive to arterial hypertension and that ventricular loading is a major determinant of the rate of myocardial recovery.

A load-independent in vivo model for evaluating therapeutic interventions in injured myocardium

1998 ◽  
Vol 275 (5) ◽  
pp. H1834-H1844 ◽  
Author(s):  
Cleveland W. Lewis ◽  
B. Zane Atkins ◽  
Kelley A. Hutcheson ◽  
Christian T. Gillen ◽  
Mary C. Reedy ◽  
...  
Keyword(s):  
Left Ventricular ◽  
Therapeutic Interventions ◽  
Segment Length ◽  
In Vivo Model ◽  
Myocardial Segment ◽  
Stroke Work ◽  
Injured Myocardium ◽  
Rabbit Myocardium ◽  
Models Of Injury

Although cardiomyocyte damage is normally irreversible, gene therapy and somatic cell transfer offer potential for improving function in damaged regions of the heart. However, in ischemic models of injury, variability in depth, size, and location of damage compromises statistical evaluation of in vivo function. We have adapted cryoablation to create a reproducible, posterior, transmural lesion within rabbit myocardium in which small changes in function are measurable in vivo. Before and at 2 and 6 wk postinjury, in vivo left ventricular intracavitary pressure and myocardial segment length were measured. Regional indexes of performance, segmental stroke work (SW), and percent systolic shortening (SS) were significantly decreased ( P < 0.001) postcryoinjury as was the slope ( M w) of the linear preload recruitable SW relationship between SW and end-diastolic segment length ( P = 0.0001). Decreased SW, SS, and M w correlated with wall thinning, loss of myocytes, presence of fibroblasts, and transmural scar formation. Reproducible changes in regional myocardial performance in vivo postcryoinjury suggest that this is a reasonable model for evaluating novel therapies for cardiovascular disease.

Quantification of regional myocardial dysfunction after acute ischemic injury

1988 ◽  
Vol 255 (1) ◽  
pp. H85-H93 ◽  
Author(s):  
D. D. Glower ◽  
J. A. Spratt ◽  
J. S. Kabas ◽  
J. W. Davis ◽  
J. S. Rankin
Keyword(s):  
Myocardial Dysfunction ◽  
Ischemic Injury ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Segment Length ◽  
Acute Ischemia ◽  
Myocardial Segment ◽  
Stroke Work ◽  
Performance Indexes ◽  
Work Area

Quantification of myocardial performance after regional ischemic injury is difficult because available performance indexes are markedly dependent on concurrent load changes. To develop a more load-insensitive index of myocardial function during ischemia, eight conscious dogs were instrumented to measure left ventricular pressure with micromanometers and myocardial segment length with ultrasonic dimension transducers. Preload was varied by transient vena caval occlusion during control conditions, after 15 min of coronary occlusion, and at intervals during 24 h of reperfusion. Acute ischemia shifted the linear relationship between segmental stroke work (SW) and end-diastolic segment length (EDL) rightward, diminishing the slope and increasing the chi-intercept. Preload recruitable work area (PRWA), defined as the area under the SW-EDL curve, reflected changes in both slope and intercept. During acute ischemia, conventional performance indexes and PRWA decreased significantly and required up to 24 h of reperfusion to return to control values. Of all parameters examined, PRWA was most responsive to prolonged ischemic dysfunction after reperfusion and was insensitive to concurrent load changes. Thus PRWA provides improved precision in quantifying of myocardial dysfunction after regional ischemic injury. This parameter should be especially useful in assessing the subtle effects of acute interventions designed to modify functional recovery.

scholarly journals Prognostic value of NT-proBNP for myocardial recovery in peripartum cardiomyopathy (PPCM)

2021 ◽  
Author(s):  
J. Hoevelmann ◽  
E. Muller ◽  
F. Azibani ◽  
S. Kraus ◽  
J. Cirota ◽  
...  
Keyword(s):  
Prognostic Value ◽  
Systolic Function ◽  
Point Of Care ◽  
Diagnostic Value ◽  
Left Ventricular ◽  
Peripartum Cardiomyopathy ◽  
Lv Function ◽  
Myocardial Recovery ◽  
End Diastolic Volume

Abstract Introduction Peripartum cardiomyopathy (PPCM) is an important cause of pregnancy-associated heart failure worldwide. Although a significant number of women recover their left ventricular (LV) function within 12 months, some remain with persistently reduced systolic function. Methods Knowledge gaps exist on predictors of myocardial recovery in PPCM. N-terminal pro-brain natriuretic peptide (NT-proBNP) is the only clinically established biomarker with diagnostic value in PPCM. We aimed to establish whether NT-proBNP could serve as a predictor of LV recovery in PPCM, as measured by LV end-diastolic volume (LVEDD) and LV ejection fraction (LVEF). Results This study of 35 women with PPCM (mean age 30.0 ± 5.9 years) had a median NT-proBNP of 834.7 pg/ml (IQR 571.2–1840.5) at baseline. Within the first year of follow-up, 51.4% of the cohort recovered their LV dimensions (LVEDD < 55 mm) and systolic function (LVEF > 50%). Women without LV recovery presented with higher NT-proBNP at baseline. Multivariable regression analyses demonstrated that NT-proBNP of ≥ 900 pg/ml at the time of diagnosis was predictive of failure to recover LVEDD (OR 0.22, 95% CI 0.05–0.95, P = 0.043) or LVEF (OR 0.20 [95% CI 0.04–0.89], p = 0.035) at follow-up. Conclusions We have demonstrated that NT-proBNP has a prognostic value in predicting LV recovery of patients with PPCM. Patients with NT-proBNP of ≥ 900 pg/ml were less likely to show any improvement in LVEF or LVEDD. Our findings have implications for clinical practice as patients with higher NT-proBNP might require more aggressive therapy and more intensive follow-up. Point-of-care NT-proBNP for diagnosis and risk stratification warrants further investigation.

scholarly journals Ventricular interaction and external constraint account for decreased stroke work during volume loading in CHF

2001 ◽  
Vol 281 (6) ◽  
pp. H2385-H2391 ◽  
Author(s):  
Thomas D. Moore ◽  
Michael P. Frenneaux ◽  
Rozsa Sas ◽  
J. J. Atherton ◽  
Jayne A. Morris-Thurgood ◽  
...  
Keyword(s):  
Diastolic Pressure ◽  
Left Ventricular ◽  
Negative Slope ◽  
Segment Length ◽  
Stroke Work ◽  
Volume Loading ◽  
End Diastolic Volume ◽  
Pulmonary Capillary ◽  
Apparent Decrease ◽  
Pericardial Pressure

The slope of the stroke work (SW)-pulmonary capillary wedge pressure (PCWP) relation may be negative in congestive heart failure (CHF), implying decreased contractility based on the premise that PCWP is simply related to left ventricular (LV) end-diastolic volume. We hypothesized that the negative slope is explained by decreased transmural LV end-diastolic pressure (LVEDP), despite the increased LVEDP, and that contractility remains unchanged. Rapid pacing produced CHF in six dogs. Hemodynamic and dimension changes were then measured under anesthesia during volume manipulation. Volume loading increased pericardial pressure and LVEDP but decreased transmural LVEDP and SW. Right ventricular diameter increased and septum-to-LV free wall diameter decreased. Although the slopes of the SW-LVEDP relations were negative, the SW-transmural LVEDP relations remained positive, indicating unchanged contractility. Similarly, the SW-segment length relations suggested unchanged contractility. Pressure surrounding the LV must be subtracted from LVEDP to calculate transmural LVEDP accurately. When this was done in this model, the apparent decrease in contractility was no longer evident. Despite the increased LVEDP during volume loading, transmural LVEDP and therefore SW decreased and contractility remained unchanged.

scholarly journals Relation of Left Ventricular Diastolic Properties to Systolic Function in Arterial Hypertension

Circulation ◽  
2000 ◽  
Vol 101 (2) ◽  
pp. 152-157 ◽  
Author(s):  
Giovanni de Simone ◽  
Rosanna Greco ◽  
GianFrancesco Mureddu ◽  
Carmela Romano ◽  
Raffaele Guida ◽  
...  
Keyword(s):  
Arterial Hypertension ◽  
Systolic Function ◽  
Left Ventricular ◽  
Diastolic Properties

Positive Inotropic and Lusitropic Effects of Triiodothyronine in Conscious Dogs with Pacing-induced Cardiomyopathy 

1997 ◽  
Vol 87 (1) ◽  
pp. 102-109 ◽  
Author(s):  
Iyad N. Jamali ◽  
Paul S. Pagel ◽  
Douglas A. Hettrick ◽  
Dermot Lowe ◽  
Judy R. Kersten ◽  
...  
Keyword(s):  
Heart Rate ◽  
Myocardial Contractility ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Segment Length ◽  
Lv Function ◽  
Baseline Heart Rate ◽  
Stroke Work ◽  
Lv Dysfunction

Background The effects of triiodothyronine (T3) on systemic hemodynamics, myocardial contractility (preload recruitable stroke work slope; Mw), and left ventricular (LV) isovolumic relaxation (time constant; tau) were examined before and after the development of pacing-induced cardiomyopathy in conscious dogs. Methods Dogs (n = 8) were chronically instrumented for measurement of aortic and LV pressure, dP/dtmax, subendocardial segment length, and cardiac output. Dogs received escalating doses (0.2, 2.0, and 20.0 mg/kg, intravenous) of T3 over 5 min at 1-h intervals, and peak hemodynamic effects were recorded 10 min after each dose and 24 h after the final dose. Dogs were then continuously paced at 220-240 beats/min for 21 +/- 2 days. Pacing was temporarily discontinued after the development of severe LV dysfunction, and administration of T3 was repeated. Results T3 produced immediate and sustained (24 h) increases (P &lt; 0.05) in Mw and dP/dtmax in dogs before the initiation of pacing, consistent with a positive inotropic effect. No changes in tau occurred. Rapid ventricular pacing over 3 weeks increased baseline heart rate (sinus rhythm) and LV end-diastolic pressure, decreased mean arterial and LV systolic pressures, and caused LV systolic (decreases in Mw and dP/dtmax) and diastolic (increases in tau) dysfunction. T3 caused immediate and sustained increases in Mw (63 +/- 7 during control to 82 +/- 7 mmHg after the 2 mg/kg dose) and decreases in tau (65 +/- 8 during control to 57 +/- 6 ms after the 20 mg/kg dose), indicating that this hormone enhanced myocardial contractility and shortened LV relaxation, respectively, in the presence of chronic LV dysfunction. In contrast to the findings in dogs with normal LV function, T3 did not affect heart rate and calculated indices of myocardial oxygen consumption and reduced LV end-diastolic pressure (27 +/- 3 during control to 20 +/- 2 mmHg after the 2 mg/kg dose) in cardiomyopathic dogs. Conclusions The findings indicate that T3 produces favorable alterations in hemodynamics and modest positive inotropic and lusitropic effects in conscious dogs with LV dysfunction produced by rapid LV pacing.

scholarly journals Prolonged effects of B-type natriuretic peptide infusion on cardiac remodeling after sustained myocardial injury

2009 ◽  
Vol 297 (2) ◽  
pp. H708-H717 ◽  
Author(s):  
Isaac George ◽  
Brad Morrow ◽  
Kai Xu ◽  
Geng-Hua Yi ◽  
Jeffrey Holmes ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Myocardial Injury ◽  
Acute Decompensated Heart Failure ◽  
Systolic Function ◽  
Ischemic Injury ◽  
Decompensated Heart Failure ◽  
Canine Model ◽  
Left Ventricular ◽  
Saline Control ◽  
Coronary Embolization

B-type natriuretic peptide (BNP) is an established first-line therapy for acute decompensated heart failure (HF), but its efficacy in preventing left ventricular (LV) remodeling after myocardial injury is unknown. The goal of this study was to evaluate the effects of BNP therapy on remodeling after ischemic injury in an awake canine model. Dogs were chronically instrumented for hemodynamics. Ischemia was created by daily coronary embolization (Embo; 3.1 × 104 beads/day) for 3 wk; 60 min after the first embolization, BNP (100 ng·kg−1·min−1; n = 6) or saline (control; n = 6) was continuously infused via a left atrial catheter for 3 wk. Hemodynamics and echocardiography were performed in an awake state at baseline, 3 wk after Embo + BNP infusion, and 4 wk after stopping Embo + BNP infusion. End-systolic elastance (Ees) and LV change in pressure over time (dP/d t) were preserved throughout Embo + BNP therapy versus control therapy (Ees: 3.76 ± 1.01 vs. 1.41 ± 0.16 mmHg/ml; LV dP/d t: 2,417 ± 96 vs. 2,068 ± 95 mmHg/s; both P < 0.05 vs. control). LV end-diastolic dimension was significantly smaller in BNP-treated dogs compared with control dogs (4.29 ± 0.10 vs. 4.77 ± 0.17 cm), and ejection fraction was maintained in treated dogs vs. control dogs (53 ± 1% vs. 46 ± 2%) (both P < 0.05 vs. control). Cyclooxygenase (COX)-2 expression in terminal LV tissue was significantly reduced after BNP therapy. Treatment with continuous infusion of BNP preserved LV geometry, improved systolic function, and prevented the progression of systolic HF after persistent ischemic injury.

Different effects of two types of ischemia on myocardial systolic and diastolic function

1985 ◽  
Vol 248 (5) ◽  
pp. H719-H728 ◽  
Author(s):  
W. J. Paulus ◽  
W. Grossman ◽  
T. Serizawa ◽  
P. D. Bourdillon ◽  
A. Pasipoularides ◽  
...  
Keyword(s):  
Coronary Occlusion ◽  
Diastolic Pressure ◽  
Lateral Wall ◽  
Regional Wall Motion ◽  
Left Ventricular ◽  
Segment Length ◽  
Myocardial Segment ◽  
Regional Wall ◽  
Wall Stiffness ◽  
Coronary Stenoses

Acute increases in left ventricular (LV) diastolic pressure relative to volume occur during angina in humans and after pacing tachycardia in dogs with coronary stenoses. In this study we assessed myocardial function following pacing tachycardia in dogs with coronary stenoses and compared it with function of the same myocardial segment during coronary occlusion. Also we calculated regional wall stiffness following pacing tachycardia in dogs with coronary stenoses. In anesthetized dogs with two-vessel critical (90%) coronary stenoses, ultrasonic crystals were implanted subendocardially to measure either anterior wall (AW) and lateral wall (LW) segment lengths (SL; n = 14) or LV wall thickness (h; n = 7). LV pressure was measured using a high-fidelity micromanometer catheter. After pacing tachycardia in dogs with two-vessel coronary stenoses, there was a substantial rise in LV end-diastolic pressure (from 6 +/- 1 to 15 +/- 1 mmHg; P less than 0.001), a slight increase in end-diastolic segment length (AWEDSL from 15.6 +/- 1.0 to 16.4 +/- 1.0 mm; p less than 0.01; and LWEDSL from 13.8 +/- 1.4 to 14.3 +/- 1.4 mm; P greater than 0.01) and a reduction of percent systolic shortening of the ischemic segments. An upward shift of the diastolic pressure-SL relation was observed in the postpacing period. During coronary occlusion the diastolic pressure-SL relation of the same segment shifted rightward, or rightward and downward, and systolic shortening became holosystolic bulging. Ischemia due to coronary stenoses plus increased O2 demand had substantially different effects on regional wall motion and segmental diastolic mechanics than did ischemia due to coronary occlusion. Over the same range of residual transmural LV diastolic pressure, the radial stiffness modulus was higher after pacing tachycardia in the presence of coronary stenoses.

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