Phasic regional myocardial inflow and outflow: comparison of theory and experiments

1990 ◽  
Vol 258 (6) ◽  
pp. H1687-H1698 ◽  
Author(s):  
R. S. Chadwick ◽  
A. Tedgui ◽  
J. B. Michel ◽  
J. Ohayon ◽  
B. I. Levy
Keyword(s):  
Arterial Pressure ◽  
Cardiac Cycle ◽  
Vagal Stimulation ◽  
Regional Blood Flow ◽  
Left Ventricular ◽  
Morphometric Measurements ◽  
Lumped Model ◽  
Arterial Inflow ◽  
Continuum Description ◽  
Theory And Experiments

We developed a theory for regional blood flow in the beating heart and validated it with measurements of coronary arterial inflow and venous outflow in the open-chest anesthetized dog. The model used measured aortic, left ventricular, and coronary sinus pressures as input data under control conditions and during long diastoles induced by vagal stimulation. A nonlinear two-compartment lumped model for each transmural layer was obtained by spatial averaging a continuum description of the myocardial microcirculation based on morphometric measurements and appropriate fluid and vascular mechanics principles. The chief results and conclusions of the study are 1) an intramyocardial time constant on the order of 1 s is required to explain the phase opposition between inflow and outflow; 2) capillary and venous perfusion are in phase with arterial pressure, and arterial flow is out of phase with arterial pressure except in superficial intramural layers; 3) subendocardial retrograde systolic flow increases with increased contractility and time constants and decreased arterial pressure; and 4) endocardial capillary and venule volume change by 5.5 and 10%, respectively, during the control cardiac cycle.

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.

Cathodic-anodal left ventricular stimulation during cardiac resynchronization therapy: haemodynamic evaluation and electrocardiographic analysis

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Gravellone ◽  
G Dell' Era ◽  
F De Vecchi ◽  
E Boggio ◽  
E Prenna ◽  
...  
Keyword(s):  
Ejection Fraction ◽  
Arterial Pressure ◽  
Cardiac Resynchronization Therapy ◽  
Right Ventricle ◽  
Single Point ◽  
Left Ventricular ◽  
Cardiac Resynchronization ◽  
Resynchronization Therapy ◽  
Biventricular Stimulation ◽  
Qrs Duration

Abstract Background Cardiac resynchronization therapy (CRT) is an established treatment for heart failure with reduced ejection fraction (HFrEF). However, one third of patients are “non responders”. Cathodic-anodal (CA) left ventricle (LV) capture is a multisite pacing occurring during CRT using both bipolar and quadripolar LV lead. It allows depolarization to arise simultaneously from the cathode and the anode of the bipole located on the LV epicardium, activating a larger volume of myocardium than cathodal pacing alone, thus potentially improving electromechanical synchrony (figure 1). We have previously proven that CA-LV stimulation is feasible and similar to bicathodic multipoint pacing (MPP) in terms of QRS wavefront activation. Purpose We aimed to evaluate both the acute intraprocedural haemodynamic and electrical effects of CA biventricular stimulation (CA-BS), comparing it with right-ventricle only pacing (Right Ventricle-Stimulation: RV-S), single-point CRT (Single Point-Biventricular Stimulation: SP-BS) and multipoint bicathodic biventricular stimulation (Multi Point-Biventricular Stimulation:MP-BS) in de novo CRT implants. Methods Ten patients candidates to CRT (LV ejection fraction ≤35% and left bundle branch block) received a quadripolar LV lead. Four pacing configurations were tested: RV-S, SP-BS, MP-BS and CA-BS, where cathode and the anode were the same electrodes used as cathodes in MP-BS. QRS duration by 12-lead ECG was defined as the time from the earliest ventricular deflection until the return to the isoelectric line. Haemodynamic assessment by radial artery catheterization using Pressure Recording Analytical Method processed the following parameters: dP/dT max (mmHg/msec), systolic arterial pressure (aPsys, mmHg), diastolic arterial pressure (aPdia, mmHg), mean arterial pressure (aPmean, mmHg), Cardiac Index (CI, l/min/m2), Stroke Volume Index (SVI, ml/min/m2). Results dP/dT max and aPmean increased significantly from RV-S to SP-BS (mean dP/dT max 0,82±0,28 versus 0,87±0,29 mmHg/msec, p=0,02; mean aPmean 89±19 versus 93±20 mmHg, p=0,01), but not from RV-S to MP-BS. Comparing RV-S to CA-BS, only aPmean exhibited a significant increase (mean aPmean 89±19 versus 92±20 mmHg, p=0,01). There were no haemodynamic differences between SP-BS, MP-BS and CA-BS. QRS duration reduced significantly from RV-S (167±10 msec) to each biventricular stimulation (135±14 msec, p=0,0002 for SP-BS; 130±17 msec, p=0,0001 for MP-BS; 129±18 msec, p=0,0002 for CA-BS) and from SP-BS to MP-BS and CA-BS (p=0,03 for both), whereas there were no difference comparing MP-BS and CA-BS. Conclusions CA-LV stimulation is not superior to single-point CRT in terms of acute haemodynamic performance, whereas it reduces the duration of ventricular electrical activation, showing an electrohaemodynamic mismatch. Long-term studies are needed to evaluate if acute electrical benefits of CA stimulation can predict chronic benefits, in terms of reverse cardiac remodelling. Cathodic-anodal left ventricular capture Funding Acknowledgement Type of funding source: None

Efferent vagal innervation of canine ventricle

1985 ◽  
Vol 248 (1) ◽  
pp. H89-H97 ◽  
Author(s):  
N. Takahashi ◽  
M. J. Barber ◽  
D. P. Zipes
Keyword(s):  
Coronary Artery ◽  
Vagal Stimulation ◽  
Left Ventricular ◽  
Constant Infusion ◽  
Epicardial Surface ◽  
Before And After ◽  
Vagal Innervation ◽  
The Subject ◽  
Infusion Of Norepinephrine ◽  
The Right

The route efferent vagal fibers travel to reach the left ventricle is not clear and was the subject of this investigation. We measured left ventricular and septal effective refractory period (ERP) changes during vagal stimulation and a constant infusion of norepinephrine, before and after phenol was applied at selected sites of the heart to interrupt efferent vagal fibers that may be traveling in that area. Phenol applied to the atrioventricular (AV) groove between the origin of the right coronary artery anteriorly to the posterior descending branch of the circumflex coronary artery completely eliminated vagal-induced prolongation of ERP in the anterior and posterior left ventricular free wall and reduced, but did not eliminate, ERP prolongation in the septum. A large (3-cm radius) epicardial circle of phenol prevented vagal-induced ERP prolongation within the circle in all dogs, while a small (1-cm radius) epicardial circle of phenol failed to prevent vagal-induced ERP changes within the circle in any dog. An intermediate (2-cm radius) circle eliminated vagal effects on ERP in 13 of 18 dogs. Arcs of phenol, to duplicate the upper portion of the circle, applied sequentially from apex to base eliminated efferent vagal effects only when painted near or at the AV groove. We conclude that the majority of efferent vagal fibers enroute to innervate the anterior and posterior left ventricular epicardium cross the AV groove within 0.25-0.5 mm (depth of phenol destruction) of the epicardial surface.(ABSTRACT TRUNCATED AT 250 WORDS)

Physiologic Analysis of Cardiac Cycle in an Implantable Impeller Centrifugal Left Ventricular Assist Device

2001 ◽  
Vol 25 (8) ◽  
pp. 613-616 ◽  
Author(s):  
Nai-Kuan Chou ◽  
Shoei-Shen Wang ◽  
Shu-Hsun Chu ◽  
Yih-Sharng Chen ◽  
Yuan-Hsiang Lin ◽  
...  
Keyword(s):  
Left Ventricular Assist Device ◽  
Ventricular Assist Device ◽  
Cardiac Cycle ◽  
Left Ventricular ◽  
Assist Device ◽  
Ventricular Assist ◽  
Left Ventricular Assist

Hyperinflation-induced cardiorespiratory failure in rats

2009 ◽  
Vol 107 (1) ◽  
pp. 275-282 ◽  
Author(s):  
Jeremy A. Simpson ◽  
Keith R. Brunt ◽  
Christine P. Collier ◽  
Steve Iscoe
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Lung Volume ◽  
Troponin T ◽  
Respiratory Acidosis ◽  
Left Ventricular ◽  
Cardiovascular Failure ◽  
Cardiorespiratory Failure ◽  
Arterial Hypoxemia ◽  
Ventricular Afterload

We previously showed that severe inspiratory resistive loads cause acute (<1 h) cardiorespiratory failure characterized by arterial hypotension, multifocal myocardial infarcts, and diaphragmatic fatigue. The mechanisms responsible for cardiovascular failure are unknown, but one factor may be the increased ventricular afterload caused by the large negative intrathoracic pressures generated when breathing against an inspiratory load. Because expiratory threshold loads increase intrathoracic pressure and decrease left ventricular afterload, we hypothesized that anesthetized rats forced to breathe against such a load would experience only diaphragmatic failure. Loading approximately doubled end-expiratory lung volume, halved respiratory frequency, and caused arterial hypoxemia and hypercapnia, respiratory acidosis, and increased inspiratory drive. Although hyperinflation immediately reduced the diaphragm's mechanical advantage, fatigue did not occur until near load termination. Mean arterial pressure progressively fell, becoming significant (cardiovascular failure) midway through loading despite tachycardia. Loading was terminated (endurance 125 ± 43 min; range 82–206 min) when mean arterial pressure dropped below 50 mmHg. Blood samples taken immediately after load termination revealed hypoglycemia, hyperkalemia, and cardiac troponin T, the last indicating myocardial injury that was, according to histology, mainly in the right ventricle. This damage probably reflects a combination of decreased O2 delivery (decreased venous return and arterial hypoxemia) and greater afterload due to hyperinflation-induced increase in pulmonary vascular resistance. Thus, in rats breathing at an increased end-expiratory lung volume, cardiorespiratory, not just respiratory, failure still occurred. Right heart injury and dysfunction may contribute to the increased morbidity and mortality associated with acute exacerbations of obstructive airway disease.

scholarly journals Assessment of aortic and mitral annuli dynamics during the cardiac cycle using speckle tracking echocardiography

2014 ◽  
Vol 1 (1) ◽  
pp. 11-16 ◽  
Author(s):  
Wenjuan Bai ◽  
Hui Li ◽  
Hong Tang ◽  
Qing Zhang ◽  
Ye Zhu ◽  
...  
Keyword(s):  
Left Ventricular Function ◽  
Ventricular Function ◽  
Speckle Tracking ◽  
Cardiac Cycle ◽  
Speckle Tracking Echocardiography ◽  
Left Ventricular ◽  
Healthy Adults ◽  
Aortic Annulus ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction

The aims of this study were i) to evaluate mitral and aortic annuli excursion, and aortomitral angle (AMA) during the cardiac cycle in healthy adults using two-dimensional speckle tracking echocardiography, ii) to assess two annuli dynamics and coupling behaviors as an integral, and iii) to detect the relation between two annuli and left ventricular ejection fraction (LVEF). A total of 74 healthy adults underwent transthoracic echocardiography. In the parasternal long-axis view, a number of points were extracted, including right coronary aortic annular, aortomitral fibrous junction, and posterior mitral annular points. The annuli excursion and AMA were measured using a speckle tracking-derived software during the cardiac cycle. During the isovolumic contraction and the isovolumic relaxation phase, annuli excursion and AMA remain stable for a short time. During the systole, annuli excursion increased sharply to the maximum, while AMA narrowed quickly to the minimum value. During the diastole, there are three patterns of decrease in annuli excursion and AMA expansion in different phases. The annuli excursion of three points correlates well with the LVEF (right coronary aortic annulus excursion, r=0.71, P<0.05; non-coronary aortic annulus excursion, r=0.70, P<0.05; posterior mitral annulus excursion, r=0.82, P<0.05). Moreover, there are positive correlations between annuli excursion and the variation of AMA (r=0.60, P<0.05). The annuli excursion and AMA have various regular patterns in healthy adults. The interactions of mitral and aortic annuli correlate with the left ventricular function. Our findings may have relevance to the evaluation of left ventricular function and presurgical planning of patients with valvular diseases.

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