Effect of activation sequence on MVO2 before and after coronary ligation

1978 ◽  
Vol 234 (3) ◽  
pp. H260-H265
Author(s):  
A. C. Kralios ◽  
T. J. Tsagaris
Keyword(s):  
Diastolic Pressure ◽  
Coronary Artery Occlusion ◽  
Systemic Arterial Pressure ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Work Index ◽  
Before And After ◽  
Ventricular Activation ◽  
Ectopic Activation ◽  
Activation Sequence

In pentobarbital-anesthetized, open-chest dogs with fixed heart rate, cardiac output, and systemic arterial pressure, ectopic ventricular activation originating from apical as compared to basilar regions of either ventricle was associated with small (3--5%) but significantly (P less than 0.005) lower myocardial O2 consumption (MVO2) and thus higher left ventricular (LV) efficiency without change in LV end-diastolic pressure (LVEDP), work index (LVWI), and LV dP/dt. Data obtained during epicardial and corresponding endocardial activation did not differ. During normal ventricular activation, MVO2 remained unchanged but LVEDP was significantly (P less than 0.005) lower, thus yielding higher LVWI and efficiency. MVO2 differences among ectopic sites were abolished after coronary artery occlusion, whereas data obtained during endocardial and epicardial on normal and ectopic activation were not affected. Thus, normal activation resulting in lower LVEDP is most efficient; apical ventricular activation is less efficient at the same MVO2P basilar is the least efficient, because both MVO2 and LVEDP are higher. Ventricular activation sequence changes do not constitute a substantial determinant of MVO2.

Effect of exercise on coronary pressure-flow relationship in hypertrophied left ventricle

1995 ◽  
Vol 269 (1) ◽  
pp. H271-H281 ◽  
Author(s):  
D. J. Duncker ◽  
J. Zhang ◽  
T. J. Pavek ◽  
M. J. Crampton ◽  
R. J. Bache
Keyword(s):  
Coronary Artery ◽  
Myocardial Perfusion ◽  
Diastolic Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Back Pressure ◽  
Pressure Flow ◽  
Pronounced Increase ◽  
Coronary Pressure

Left ventricular (LV) hypertrophy (LVH) secondary to chronic pressure overload is associated with increased susceptibility to myocardial hypoperfusion and ischemia during exercise. The present study was performed to determine whether exercise causes alterations in minimum coronary resistance or effective back pressure [coronary pressure at zero flow (Pzf)] that limit maximum myocardial perfusion in the hypertrophied heart. Ascending aortic banding in 7 dogs increased the LV weight-to-body weight ratio to 7.7 +/- 0.3 g/kg compared with 4.6 +/- 0.2 g/kg in 11 normal dogs (P < 0.01). Maximum coronary vasodilation was produced by intracoronary infusion of adenosine. Under resting conditions, the slope of the pressure-flow relationship (conductance) was significantly lower in the LVH animals than in the normal dogs (7.2 +/- 0.8 vs. 11.9 +/- 0.8 x 10(-2) ml.min-1.g-1.mmHg-1; P < 0.01); the slope correlated with the degree of hypertrophy r = 0.74; P < 0.001). The Pzf measured during total coronary artery occlusion (Pzf,measured) was significantly elevated in LVH compared with normal dogs (25.6 +/- 2.2 vs. 13.0 +/- 1.2 mmHg; P < 0.01); Pzf,measured was positively correlated (r = 0.78, P < 0.0005) with LV end-diastolic pressure measured during total coronary artery occlusion (9.0 +/- 1.1 mmHg in normal dogs and 22.2 +/- 3.2 mmHg in LVH dogs; P < 0.01). Graded treadmill exercise to maximum heart rates of 210 +/- 9 and 201 +/- 8 beats/min in normal and LVH animals, respectively, caused similar decreases in the slope of the pressure-flow relationship in LVH (from 7.7 +/- 0.9 to 6.1 +/- 0.8 x 10(-2) ml.min-1.g-1.mmHg-1; P < 0.01) and normal dogs (from 11.9 +/- 0.8 to 10.0 +/- 0.7 x 10(-2) ml.min-1.g-1.mmHg-1; P < 0.01). However, exercise-induced increases in Pzf,measured were significantly greater in the LVH animals (from 25.6 +/- 2.2 to 40.8 +/- 2.1 mmHg; P < 0.01) than in normal animals (from 13.0 +/- 1.2 to 24 +/- 2.1 mmHg; P < 0.01) (P < 0.01 LVH vs. normal). The greater increase in Pzf paralleled a more pronounced increase in LV end-diastolic pressure in the LVH dogs from 22.2 +/- 3.2 to 39.1 +/- 2.7 mmHg) than in normal dogs from 9.0 +/- 1.1 to 14.2 +/- 2.0 mmHg). The results suggest that exaggerated increases in filling pressure during exercise in the hypertrophied left ventricles contributed to impairment of myocardial perfusion during exercise by augmenting the back pressure, which opposes coronary flow.(ABSTRACT TRUNCATED AT 400 WORDS)

Abstract 3341: Human Coronary Collaterals Inversely Correlate with Indices of Ischemic Left Ventricular Diastolic Dysfunction during Coronary Balloon Occlusion.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Stephen P Hoole ◽  
Paul A White ◽  
Patrick M Heck ◽  
Michael O’Sullivan ◽  
Sarah C Clarke ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Diastolic Dysfunction ◽  
Diastolic Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Balloon Occlusion ◽  
Flow Index ◽  
Collateral Flow ◽  
Coronary Collaterals

Background: Coronary collaterals are thought to reduce myocardial ischemia during coronary artery occlusion. Coronary collaterals, defined angiographically, reduce end diastolic LV dilatation during coronary occlusion. However, counter to a role in reducing ischemia, they appear to be associated with an increase in LV end diastolic pressure. These changes may be explained if coronary collaterals act as an external LV scaffold. We aimed to re-evaluate this relationship by simultaneously measuring coronary collaterals and LV contractility quantitatively. Methods: Ten patients with normal LV function and single vessel coronary disease awaiting PCI were recruited. Collateral flow index, derived by pressure-wire measurement (CFI p = [P distal (occluded) − P venous ] / [P aorta − P venous ]) and change in LV end-diastolic pressure (LVEDP), volume (LVEDV) and Tau, measured by an LV cavity conductance catheter, were recorded simultaneously after 1 minute coronary balloon occlusion. A mean of 5 cardiac cycles was analyzed. Measurements were repeated after a recovery period of 30 minutes. Results: Percentage change in LVEDP and Tau inversely correlated with CFI p (ΔLVEDP vs. CFI p : y = −216.6x +63.4, r = 0.57, p=0.01; ΔTau vs. CFI p : y = −64.1x + 27.8, r = 0.47, p<0.05) (Figure ). There was also an inverse relationship between ΔLVEDV vs. CFI p (y = −8.4x + 1.5, r = 0.35, p = 0.15). Conclusion: Coronary collaterals inversely correlate with LV end diastolic stiffness and dilatation after 1 minute of coronary artery occlusion. This reflects a role in reducing ischemic LV diastolic dysfunction, by providing an alternative blood supply to the LV myocardium, rather than acting as an LV scaffold.

Preserved ventricular contractility in infarcted mouse heart overexpressing β2-adrenergic receptors

2000 ◽  
Vol 279 (5) ◽  
pp. H2456-H2463 ◽  
Author(s):  
Xiao-Jun Du ◽  
Xiao-Ming Gao ◽  
Garry L. Jennings ◽  
Anthony M. Dart ◽  
Elizabeth A. Woodcock
Keyword(s):  
Adrenergic Receptors ◽  
Diastolic Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Mouse Heart ◽  
Ventricular Contractility ◽  
Wild Type ◽  
Rate Of Increase ◽  
Fractional Shortening

Effects of cardiac specific overexpression of β2-adrenergic receptors (β2-AR) on the development of heart failure (HF) were studied in wild-type (WT) and transgenic (TG) mice following myocardial infarction (MI) by coronary artery occlusion. Animals were studied by echocardiography at weeks 7 to 8 and by catheterization at week 9 after surgery. Post-infarct mortality, due to HF or cardiac rupture, was not different among WT mice, and there was no difference in infarct size (IS). Compared with the sham-operated group (all P < 0.01), WT mice with moderate (<36%) and large (>36%) IS developed lung congestion, cardiac hypertrophy, left ventricular (LV) dilatation, elevated LV end-diastolic pressure (LVEDP), and suppressed maximal rate of increase of LV pressure (LV dP/d t max) and fractional shortening (FS). Whereas changes in organ weights and echo parameters were similar to those in infarcted WT groups, TG mice had significantly higher levels of LV contractility in both moderate (dP/d t max 4,862 ± 133 vs. 3,694 ± 191 mmHg/s) and large IS groups (dP/d t max4,556 ± 252 vs. 3,145 ± 312 mmHg/s, both P< 0.01). Incidence of pleural effusion (36% vs. 85%, P < 0.05) and LVEDP levels (6 ± 0.3 vs. 9 ± 0.8 mmHg, P < 0.05) were also lower in TG than in WT mice with large IS. Thus β2-AR overexpression preserved LV contractility following MI without adverse consequence.

Innate protection of baboon myocardium: effects of coronary artery occlusion and reperfusion

1996 ◽  
Vol 270 (5) ◽  
pp. H1812-H1818 ◽  
Author(s):  
Y. T. Shen ◽  
J. T. Fallon ◽  
M. Iwase ◽  
S. F. Vatner
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Infarct Size ◽  
Diastolic Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Area At Risk ◽  
Protective Mechanisms ◽  
Reperfusion Period

To determine whether the extent of myocardial infarction differs in conscious baboons and pigs, both devoid of performed collaterals, the effects of 40 and 90 min of coronary artery (CA) occlusion (O) both followed by 4-7 days of CA reperfusion (R) were examined in both species. CAO reduced subendocardial and subepicardial blood flows similarly, almost to zero, in baboons and pigs for the entire CAO period. At 24 h of CAR, subendocardial blood flow had almost returned to pre-CAO control levels in baboons but remained significantly depressed in pigs. The major difference in hemodynamics during CAO and CAR was in left ventricular end-diastolic pressure, which rose by 6 +/- 1 mmHg in pigs over the initial 24-h reperfusion period but did not change significantly in baboons. These data on recovery of subendocardial blood flow and left ventricular end-diastolic pressure suggest larger infarcts in pigs than in baboons. Indeed, infarct size expressed as a function of area at risk (IF/AAR) was significantly greater (P <0.05) in pigs (53 +/- 4.9%) than in baboons (17 +/- 2.9%) with 90 min of CAO and 4-7 days of CAR. With 40 min of CAO and 4-7 days of CAR, IF/AAR was 46 +/- 3.6% in pigs, whereas in baboons the IF/AAR was minimal, i.e., 2 +/- 0.6%. Thus pigs and baboons were characterized by minimal coronary collateral circulation, but infarct size was significantly less in conscious baboons than in conscious pigs. Potentially, these differences could be explained, in part, by natural protective mechanisms and/or less reperfusion injury in primates. These results in primates may also help explain the salutary effects of CAR in patients at intervals longer than have been demonstrated to be beneficial in other experimental animals.

Effects of myocardial ischemia on regional function and stiffness in conscious dogs

1987 ◽  
Vol 252 (1) ◽  
pp. H110-H117 ◽  
Author(s):  
J. Amano ◽  
J. X. Thomas ◽  
M. Lavallee ◽  
I. Mirsky ◽  
D. Glover ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Diastolic Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Segment Length ◽  
Stiffness Constant ◽  
Diastolic Stiffness ◽  
Velocity Of Shortening

The extent to which cardiac nerves influence responses of regional ventricular function to acute myocardial ischemia was investigated in conscious dogs with intact cardiac innervation (N) and dogs with chronic cardiac denervation (D). Following coronary artery occlusion (CAO) left ventricular (LV) end-diastolic pressure increased more (P less than 0.01) in D (18 +/- 3.2 mmHg) than in N dogs (3.4 +/- 0.7 mmHg), whereas heart rate increased more in N (32 +/- 4.8 beats/min) than in D dogs (16 +/- 3.0 beats/min). In nonischemic zones of D dogs there were greater increases, P less than 0.05, in end-diastolic segment length, systolic segment shortening, and velocity of shortening than in N dogs. In ischemic zones, significantly greater increases in end-diastolic segment length were also observed in the D group, but similar reductions in segmental shortening occurred in both N (-116 +/- 2.8%) and D (-108 +/- 5.2%) dogs. The time constant of isovolumic relaxation was not different in the two groups. However, in ischemic zones of N dogs myocardial stiffness constant (k) increased by 109 +/- 24 from 33 +/- 4.9 and end-diastolic stiffness (Eed) rose by 1527 +/- 310 from 253 +/- 34 mmHg, whereas k increased significantly less (P less than 0.05) in D dogs. Eed of ischemic zones also rose significantly less (P less than 0.05) in D dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Left ventricular pseudoaneurysm: an inadvertent consequence of COVID-19—a case report

2021 ◽  
Vol 5 (7) ◽  
Author(s):  
Stephen Brennan ◽  
Saadah Sulong ◽  
Matthew Barrett
Keyword(s):  
Multimodal Imaging ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Medical Complications ◽  
Mechanical Complication ◽  
Resonance Imaging ◽  
Left Ventricular Pseudoaneurysm ◽  
Non Invasive ◽  
Case Summary

Abstract Background Left ventricular pseudoaneurysm (LVP) is an uncommon but serious mechanical complication of acute myocardial infarction (AMI). The immediate medical complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are well recognized, but its indirect effect on patients and healthcare systems is potentially less perceivable. Case summary In this report, a 72-year-old man who was anxious about attending hospital during the SARS-CoV-2 pandemic was eventually found to have a total right coronary artery occlusion after a delayed emergency department presentation. He ultimately developed severe symptomatic heart failure and cardiac magnetic resonance imaging (CMR) revealed that a large LVP with concomitant severe ischaemic mitral regurgitation had evolved from his infarct. The patient was successfully discharged home after the surgical replacement of his mitral valve and repair of his LVP. Discussion This case highlights a salient downstream effect of Coronavirus disease 2019 (COVID-19): the delay in presentation, diagnosis, and management of common treatable conditions such as AMI. It also underscores the importance of non-invasive multimodal imaging on the timely identification of the mechanical complications of AMI. In particular, CMR can play a crucial role in the characterization and management of LVP.

Ventricular function in the newborn lamb

1965 ◽  
Vol 208 (5) ◽  
pp. 931-937 ◽  
Author(s):  
S. Evans Downing ◽  
Norman S. Talner ◽  
Thomas H. Gardner
Keyword(s):  
Ventricular Function ◽  
Diastolic Pressure ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Ventricular Mechanics ◽  
Inotropic State ◽  
Ejection Rate ◽  
Norepinephrine Infusion

The present study was initiated with the objective of evaluating in the newborn those aspects of ventricular mechanics which form the basis of the Frank-Starling relation, and which permit a determination of changes in the inotropic state of the heart. Left ventricular function was studied in lambs, 12 hr to 5 days old, utilizing a preparation designed to permit control and measurement of systemic arterial pressure (AP), cardiac output, heart rate (HR), and temperature. Continuous measurements of arterial Po2 and pH were made. These data permitted the construction of ventricular function curves relating stroke volume, mean ejection rate, and stroke work and power to left ventricular end-diastolic pressure, at constant AP and HR. In all preparations the Frank-Starling relation was found to be operative. Norepinephrine infusion, 1–2 µg/kg per min, resulted in a substantial increment of both force and speed parameters, thereby demonstrating the ability of the newborn heart to alter its inotropic state. Severe metabolic acidosis did not inhibit the response of the myocardium to norepinephrine.

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