Redistribution of myocardial fiber strain and blood flow by asynchronous activation

1990 ◽  
Vol 259 (2) ◽  
pp. H300-H308 ◽  
Author(s):  
F. W. Prinzen ◽  
C. H. Augustijn ◽  
T. Arts ◽  
M. A. Allessie ◽  
R. S. Reneman
Keyword(s):  
Blood Flow ◽  
Right Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Electrical Activation ◽  
Ventricular Wall ◽  
Activation Time ◽  
The Right ◽  
Ejection Phase

Hearts of 11 anesthetized open-chest dogs were paced from the right atrium (RA), right ventricular outflow tract (RVOT), and left ventricular apex (LVA). Maps of the sequence of electrical activation (192 electrodes), fiber strain (video technique), and blood flow (microsphere technique) in the epicardial layers were obtained from a 15- to 20-cm2 area of the anterior left ventricular wall. Electrical asynchrony in this area was 10 +/- 5 (RA), 52 +/- 12 (RVOT), and 30 +/- 16 ms (LVA, mean +/- SD, P less than 0.05 for RVOT and LVA compared with RA). Epicardial fiber strain during the ejection phase was uniformly distributed during RA pacing. However, during ventricular pacing it ranged from 13 +/- 33% (RVOT) and 23 +/- 29% (LVA) of the value during RA pacing in early-activated regions to 268 +/- 127% (RVOT) and 250 +/- 130% (LVA) of this value in late-activated regions. Epicardial blood flow ranged from 81 +/- 22% (RVOT) and 79 +/- 23% (LVA) in early-activated regions to 142 +/- 42% (RVOT) and 126 +/- 22% (LVA) in late activated regions. In all above values P less than 0.05 compared with RA. During RVOT pacing, gradients of epicardial electrical activation time, fiber strain, and blood flow pointed in the same direction. Compared with RVOT pacing, during LVA pacing all gradients were opposite in direction, and the gradients of electrical activation time and blood flow appeared to be smaller. These results indicate that timing of electrical activation is an important determinant for the distribution of fiber strain and blood flow in the left ventricular wall.

Gradients in fiber shortening and metabolism across ischemic left ventricular wall

1986 ◽  
Vol 250 (2) ◽  
pp. H255-H264 ◽  
Author(s):  
F. W. Prinzen ◽  
T. Arts ◽  
G. J. van der Vusse ◽  
W. A. Coumans ◽  
R. S. Reneman
Keyword(s):  
Blood Flow ◽  
Perfusion Pressure ◽  
Venous Blood ◽  
Creatine Phosphate ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Arterial Stenosis ◽  
Ventricular Wall ◽  
Metabolic Disturbances ◽  
Ejection Phase

Blood flow, metabolism, and fiber shortening in various layers of left ventricular wall were studied during the initial 5 min of ischemia. In open-chest dogs (n = 51) ischemia was induced by coronary arterial stenosis (median value of mean perfusion pressure distal to stenosis 3.3 kPa). Epicardial deformation measurements with an inductive technique allowed estimation of fiber shortening in inner (eendo,est) and outer layers (eepi) of left ventricular free wall during the ejection phase. The decrease of eendo,est occurred within a few seconds after onset of stenosis, whereas eepi started to decrease 30 s later. After 1 min, eendo,est diminished to zero concomitantly with a reduction of blood flow and creatine phosphate content in the inner layers by 68 and 46%, respectively. In contrast a 60% reduction of eepi was associated with a decrease in blood flow of only 32% and no significant decrease in creatine phosphate in the outer layers. H+ and inorganic phosphate were released simultaneously into the local venous blood starting within 1 min of ischemia. During the initial 5 min of ischemia the content of ATP and glycogen remained unchanged across the ischemic wall. Present results indicate that the decrease of fiber shortening in the inner layers is associated with severe metabolic dearrangements, as reflected by the depletion of creatine phosphate. They also indicate that, during coronary arterial stenosis, impaired fiber shortening in the outer layers may result from the impairment of mechanical function in the inner layers, rather than from metabolic disturbances in the outer layers themselves.

scholarly journals P180 Pulmonary valve stenosis and pulmonary trunk aneurysm in old female with syncope

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
C Fiore ◽  
A M F Ali ◽  
T Kemaloglu Oz ◽  
G Cagnazzo ◽  
M Melone ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Pulmonary Valve ◽  
Right Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Pulmonary Trunk ◽  
Aortic Aneurysms ◽  
Heart Team ◽  
The Right

Abstract A 77-year-old female, known hypertensive and dyslipidemic on treatment presented with three episodes of syncope in the last two months. On examination; there was grade 4/6 harsh systolic murmur on the lateral sternal border. Transthoracic echocardiography was difficult because of mesocardia and abnormal rotation of the heart due to enlarged right sided chambers. There is mild left ventricular hypertrophy with normal ejection fraction, no left sided valvular disease. The right ventricle was hypertrophied and dilated with normal RV function. The pulmonary valve was thickened with significant systolic flow aliasing through the valve with significant regurgitation and huge main pulmonary trunk aneurysm (59 mm at its wideset diameter) (Figure 1). Transthoracic approach did not allow a correct alignment of the Doppler CW and the correct estimate of pulmonary valvulopathy; TEE was performed with a correct visualization of the valve in deep transgastric projection at 90 degrees. The valve was thickened, fibrotic, degenerated with systolic doming of leaflets (Figure 2) and peak systolic gradient ∼ 70 mmHg (Figure 3). 3D reconstruction of the valve showed a tricuspid valve (Figure 4) with a valve area ∼ 0.9 cm2 using planimetry in MPR (Figure 5). CT scan was performed which confirmed the main pulmonary trunk aneurysm ∼ 60 mm (Figure 6). Therefore, in light of the clinical and instrumental picture, the patient was referred to heart team discussion for the plan of surgical intervention. Discussion According to the ESC guidelines for grown up congenital heart disease in 2010, this pulmonary valve should be intervened upon as it is severe symptomatic PS (1), but there are 2 problems with this case; the first is significant associated PR, so no place for balloon dilatation here, the second problem is the pulmonary artery aneurysm (PAA). The dilemma of management of pulmonary PAA is that all the available data are about aortic aneurysms. Indications for intervention for PAA include: Absolute PAA diameter ≥ 5.5 cm, Increase in the diameter of the aneurysm of ≥ 0.5 cm in 6 mo, Compression of adjacent structures, Thrombus formation in the aneurysm sack, Evidence of valvular pathologies or shunt flow Verification of PAH, Signs of rupture or dissection (2). Surgery could include: Aneurysmorrhaphy only decreases the diameter of the vessel (3). Aneurysmectomy and repair or replacement of the right ventricular outflow tract is commonly used technique recently and mostly suits connective tissue disorders (6). Also, Replacement of the PA and the pulmonary trunk with a conduit (Gore-Tex or Dacron tubes, homografts, or xenografts) starting in the right ventricular outflow tract with replacement of the pulmonary valve (4). Conclusion PAA management is currently challenging because there are no clear guidelines on its optimal treatment. The presence of significant pulmonary valve dysfunction could affect the decision making of the associated PAA management. Abstract P180 Figure.

Parasympathetic control of transmural coronary blood flow in dogs

1985 ◽  
Vol 249 (2) ◽  
pp. H337-H343 ◽  
Author(s):  
J. V. Reid ◽  
B. R. Ito ◽  
A. H. Huang ◽  
C. W. Buffington ◽  
E. O. Feigl
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Vagal Stimulation ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Regional Myocardial Blood Flow ◽  
Ventricular Wall ◽  
Flow Ratio ◽  
Outer Flow

The transmural distribution of coronary blood flow was studied during vagal stimulation in closed-chest, morphine- and alpha-chloralose-anesthetized dogs. The left main coronary artery was cannulated and perfused at constant pressure. Bradycardia during vagal stimulation was prevented by atrioventricular heart block and ventricular pacing. Beta-adrenergic receptors were blocked with propranolol (1 mg/kg iv), and aortic pressure was stabilized by means of a pressure reservoir. Regional myocardial blood flow was measured with 9-micron radioactive microspheres during vagal stimulation and during intracoronary acetylcholine infusion. Vagal stimulation increased coronary blood flow uniformly across the left ventricular wall. In contrast, intracoronary acetylcholine infusion, at a rate selected to increase total flow to the same degree, vasodilated the subendocardium more than the subepicardium, increasing the inner/outer blood flow ratio. It is concluded that both vagal activation and acetylcholine produce coronary vasodilation that is independent of left ventricular preload, afterload, and heart rate. Acetylcholine vasodilation preferentially vasodilates the subendocardium, increasing the inner/outer flow ratio, but vagal stimulation produces uniform vasodilation across the left ventricular wall.

scholarly journals Discovery of a Symptomatic Left Anomalous Coronary Artery from the Opposite Sinus and Postoperative Considerations

2009 ◽  
Vol 2009 ◽  
pp. 1-3 ◽  
Author(s):  
Ahmad Slim ◽  
John Thurlow ◽  
Jennifer Blevins ◽  
Shaun Martinho ◽  
Brian Markelz
Keyword(s):  
Coronary Artery ◽  
Right Ventricular Outflow Tract ◽  
Rare Condition ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Anomalous Origin ◽  
Complex Anatomy ◽  
Increased Risk ◽  
The Right

This is the case of an 18 year old active duty soldier with symptoms of exertional chest pressure and syncope who was found to have anomalous origin of the left main coronary artery (LMCA) from the right coronary cusp (RCC) traveling partially between the great vessels before taking a septal approach between the left ventricular outflow tract (LVOT) and the right ventricular outflow tract (RVOT). Anomalous origin of coronary arteries is a rare condition that carries an increased risk of angina, myocardial ischemia, and sudden cardiac death (SCD). Surgical treatment of such anomalies with both high and lower risk features can be challenging, and traditional benefit from surgical correction may not be achieved due to complex anatomy. As evident by our patient, this rare condition even though benign from sudden death standpoint could be debilitating despite best efforts and available resources.

The effect of graded coronary stenosis on myocardial blood flow and left ventricular wall motion

1977 ◽  
Vol 72 (5) ◽  
pp. 479-491 ◽  
Author(s):  
M. Nakamura ◽  
H. Matsuguchi ◽  
A. Mitsutake ◽  
Y. Kikuchi ◽  
A. Takeshita ◽  
...  
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Coronary Stenosis ◽  
Wall Motion ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Left Ventricular Wall Motion ◽  
Ventricular Wall Motion

scholarly journals Right Ventricular Outflow Tract Tachycardia with Structural Abnormalities of the Right Ventricle and Left Ventricular Diverticulum

2015 ◽  
Vol 2015 ◽  
pp. 1-3
Author(s):  
Bortolo Martini ◽  
Nicola Trevisi ◽  
Nicolò Martini ◽  
Li Zhang
Keyword(s):  
Right Ventricle ◽  
Right Ventricular ◽  
Right Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Ventricular Diverticulum ◽  
Right Ventricular Wall ◽  
Left Ventricular Diverticulum ◽  
The Right

A 43-year-old woman presented to the emergency room with a sustained ventricular tachycardia (VT). ECG showed a QRS in left bundle branch block morphology with inferior axis. Echocardiography, ventricular angiography, and cardiac magnetic resonance imaging (CMRI) revealed a normal right ventricle and a left ventricular diverticulum. Electrophysiology studies with epicardial voltage mapping identified a large fibrotic area in the inferolateral layer of the right ventricular wall and a small area of fibrotic tissue at the anterior right ventricular outflow tract. VT ablation was successfully performed with combined epicardial and endocardial approaches.

Regulation of coronary flow

2021 ◽  
pp. 11-13
Author(s):  
Nico Bruining ◽  
Eric Boersma ◽  
Dirk J. Duncker
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Arterial Blood ◽  
Arterial Inflow ◽  
Systolic Phase ◽  
Vascular Beds

This chapter describes the regulation of coronary blood flow. The left ventricle generates the systemic arterial blood pressure that is required to maintain coronary blood flow. The coronary circulation is unique among regional vascular beds in that its perfusion is impeded during the systolic phase of the cardiac cycle by the surrounding contracting cardiac muscle. Systolic contraction increases left ventricular wall tension and compresses the intramyocardial microvessels, thereby impeding coronary arterial inflow. This compression is not uniformly distributed across the left ventricular wall, resulting in a redistribution of blood flow from the subendocardium to subepicardium.

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