Reply to Comment on "Effect of Transcatheter Edge-to-Edge Repair on Left Ventricular Flow Features".

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Regional coronary blood flow in awake resting and pharmacologically stressed dogs

Regional myocardial blood flow was measured in nine dogs at rest and during three levels of treadmill exercise by using left atrial injections of 7-10-mum radioactive microspheres. At rest, heart rate was 76 plus or minus 3 beats/min (mean plus or minus SEM), mean left ventricular myocardial flow was 0.94 plus or minus 0.09 ml/min/g and endocardial flow (endo) exceeded epicardial flow (epi) in all regions (endo/epi equals 1.12-1.33). When treadmill exercise was regulated to increase heart rates from 152 plus or minus 3 to 190 plus or minus 3 to 240 plus or minus 6 beats/min, myocardial blood flow (MBF) to all regions of the left ventricle increased linearly with heart rate (HR) from 1.83 plus or minus 0.11 to 2.75 plus or minus 0.22 to 3.90 plus or minus 0.26 ml/min/g (MBF EQUALs 0.0175 HR - 0.523 PLUS OR MINUS 0.614, R EQUALS 0.87). Exercise abolished the gradient of blood flow favoring the left ventricular endocardium at rest, so that the endo/epi flow ratios were not significantly different from 1.00. Right ventricular flows were consistently less than corresponding left ventricular flows, but showed a similar linear increase with heart rate. Right ventricular endo/epi ratios were not different from 1.00 either at rest or during exercise. Thus, exercise resulted in increased myocardial blood flow to all regions of the left and right ventricles with maintenance of subendocardial flow equal to subepicardial flow.

Cardiac remodeling, after a myocardial insult, often causes progression to heart failure. The relationship between alterations in left ventricular blood flow, including kinetic energy (KE), and remodeling is uncertain. We hypothesized that increasing derangements in left ventricular blood flow would relate to (1) conventional cardiac remodeling markers, (2) increased levels of biochemical remodeling markers, (3) altered cardiac energetics, and (4) worsening patient symptoms and functional capacity. Methods Thirty-four dilated cardiomyopathy patients, 30 ischemic cardiomyopathy patients, and 36 controls underwent magnetic resonance including 4-dimensional flow, BNP (brain-type natriuretic peptide) measurement, functional capacity assessment (6-minute walk test), and symptom quantification. A subgroup of dilated cardiomyopathy and control subjects underwent cardiac energetic assessment. Left ventricular flow was separated into 4 components: direct flow, retained inflow, delayed ejection flow, and residual volume. Average KE throughout the cardiac cycle was calculated. Patients had reduced direct flow proportion and direct-flow average KE compared with controls ( P<0.0001). The residual volume proportion and residual volume average KE were increased in patients ( P<0.0001). Importantly, in a multiple linear regression model to predict the patient's 6-minute walk test, the independent predictors were age (β=-0.3015; P=0.019) and direct-flow average KE (β=0.280, P=0.035; R2 model, 0.466, P=0.002). In contrast, neither ejection fraction nor left ventricular volumes were independently predictive. This study demonstrates an independent predictive relationship between the direct-flow average KE and a prognostic measure of functional capacity. Intracardiac 4-dimensional flow parameters are novel biomarkers in heart failure and may provide additive value in monitoring new therapies and predicting prognosis.

The measurement of coronary blood flow, oxygen consumption, and efficiency of the left ventricle in man

The present study was designed to determine whether the antilipolytic agent β-pyridylcarbinol modifies left ventricular blood flow distribution. It has been shown that the administration of this agent during isoproterenol infusion reduced both myocardial oxygen consumption and myocardial free fatty acid uptake. Although attributed to a decrease in myocardial free fatty acid uptake, the reduction in myocardial oxygen consumption might also be due to a modification in left ventricular blood flow distribution induced by β-pydidyiearbinol. To verify this possibility left ventricular blood flow distribution was measured with radioactive microspheres in 10 anesthetized dogs during control, during an infusion of isoproterenol (0.2 μg∙kg−1∙min−1) alone, and during an isoproterenol plus β-pyridylcarbinol infusion (0.1 mg∙kg−1∙min−1). In comparison with the control observations, isoproterenol infusion induced a significant increase of 37% in heart rate and of nearly 100% in myocardial free fatty acid uptake, myocardial oxygen consumption, and coronary blood flow, but did not affect the left ventricular blood flow distribution. The addition of β-pyridylcarbinol to the isoproterenol infusion did not cause any significant changes in left ventricular blood flow distribution, although it reduced myocardial free fatty acid uptake by 67% (p &lt; 0.01). Despite this reduction, myocardial oxygen consumption did not change. However, in dogs with a myocardial oxygen uptake above 12.5 mL∙min−1∙100 g−1 during isoproterenol infusion, there was a reduction in myocardial oxygen consumption when β-pyridylcarbinol was added, without significant change in left ventricular blood flow distribution. The present findings reveal that β-pyridylcarbinol does not modify left ventricular blood flow distribution and that the determinant role of free fatty acids on myocardial oxygen consumption is restricted to conditions with increased myocardial demand.

Artificial heart valve replacement is recognized as the most effective method for treating valvular heart disease. Presently, the bileaflet mechanical heart valve is the predominant type utilized. Nonetheless, complications are known to arise following valve replacement surgery, mostly attributable to deviations in the left ventricular blood flow pattern instigated by the dysfunction of the bileaflet mechanical valve. However, the impact of mitral valve leaflet dysfunction on left ventricular hemodynamics has not been studied in depth. Hence, to approximate the physiological conditions of the left ventricular flow and pressure, a left heart circulation pulsatile flow system was devised. The time-resolved particle image velocimetry method was employed to evaluate the left ventricular blood flow under standard working conditions of the bileaflet mechanical valve and in the case where one of the valve leaflets is determined to be functionally impaired. The experimental results reveal that the normally functioning bileaflet valve manifests a tri-jet flow pattern, with intense jets on both sides generating two expansive vortices. Conversely, when one of the valve leaflets is impaired, the tri-jet flow metamorphoses into a bi-jet flow, coupled with augmented velocity. In both instances, the jets traverse along the ventricular model wall and alter their direction subsequent to passing the apex. Consequently, the employment of bileaflet valves culminates in a multifaceted left ventricular blood flow pattern. Furthermore, the valve leaflet dysfunction escalates shear stress, a condition that could potentially instigate damage to blood cells. The insights gained from this study can potentially guide the improved design of the mechanical bivalve.

Assessment of sex differences in ventricular-vascular coupling of left ventricular and aortic flow derived from 4D flow MRI in healthy, young adults

Blood glucose alterations prior to cerebral ischaemia are associated with poor neurologic outcome, possibly due to extensive lactic acidosis or energy failure. Cerebral effects of hyper- or hypoglycaemia during cardiopulmonary resuscitation (CPR) are less well known. In addition, little information is available concerning cardiac effects of blood glucose alterations. The aim of this study was to evaluate the effects of pre-cardiac-arrest hypo- or hyper-glycaemia compared to normoglycaemia upon haemodynamics, cerebral blood flow (CBF) and metabolism (CMRO2), and regional cardiac blood flow during CPR subsequent to 3 min of cardiac and respiratory arrest and after restoration of spontaneous circulation. After approval by the State Animal Investigation Committee, 29 mechanically ventilated, anaesthetised pigs were instrumented for haemodynamic monitoring and blood flow determination by the radiolabeled microsphere technique. The animals were randomly assigned to one of three groups: in group 1 (n = 9) blood glucose was not manipulated; in group II (n = 10) blood glucose was increased by slow infusion of 40% glucose to 319 +/- 13 mg/dl; in group III (n = 10) blood glucose was lowered by careful titration with insulin to 34 +/- 2 mg/dl. After 3 min of untreated ventricular fibrillation and respiratory arrest, CPR (chest compressor/ventilator (Thumper) and epinephrine infusion) was commenced and continued for 8 min. Thereafter, defibrillation was attempted, and if successful, the animals were observed for another 240 min. Cerebral perfusion pressure (CPP), CBF, CMRO2, coronary perfusion pressure (CorPP), and regional cardiac blood flow were determined at control, after 3 min of CPR, and at 10.30, and 240 min post-CPR. In group 1. 4/9 animals (44%) could be successfully resuscitated; in group II 4/10 (40%); and in group III 0/10 (0%). Prior to cardiac arrest, mean arterial pressure, CPP, and CorPP in group III were significantly lower compared to groups I and II. In group I. CPP during CPR was 26 +/- 6 mmHg; CBF 31 +/- 9 ml/ min/100g CMRO2 3.8 +/- 1.2 ml/ min/100 g; CorPP 18 +/- 5 mmHg; and left ventricular (LV) flow 35 +/- 15 ml/min/100 g. In group II; CPP = 21 +/- 5; CBF 21 +/- 7; CMRO2 1.8 +/- 0.8; CorPP 16 +/- 6; and LV flow 22 +/- 9; and in group III: CPP 15 +/- 3; CBF 11 +/- 8; CMRO2 1.5 +/- 1.1; CorPP 4 +/- 2; and LV flow 19 +/- 10. During the 240-min post-resuscitation period, there were no differences in CBF, CMRO2, or LV flow between groups I and II. Hypoglycaemia prior to cardiac arrest appears to be predictive for a poor cardiac outcome, whereas hyperglycaemia does not impair resuscitability compared to normoglycaemia. In addition, hyperglycaemia did not affect LV flow, CBF, or CMRO2. However, it has to be kept in mind that haemodynamics and organ blood flow do not permit conclusions with respect to functional neurologic recovery or histopathologic damage to the brain, which is very likely to be associated with hyperglycaemia.

BackgroundBranch pulmonary artery (PA) stenosis (PAS) commonly occurs in patients with congenital heart disease (CHD). Prior studies have documented technical success and clinical outcomes of PA stent interventions for PAS but the impact of PA stent interventions on ventricular function is unknown. The objective of this study was to utilize 4D flow cardiovascular magnetic resonance (CMR) to better understand the impact of PAS and PA stenting on ventricular contraction and ventricular flow in a swine model of unilateral branch PA stenosis.Methods18 swine (4 sham, 4 untreated left PAS, 10 PAS stent intervention) underwent right heart catheterization and CMR at 20 weeks age (55 kg). CMR included ventricular strain analysis and 4D flow CMR.Results4D flow CMR measured inefficient right ventricular (RV) and left ventricular (LV) flow patterns in the PAS group (RV non-dimensional (n.d.) vorticity: sham 82 ± 47, PAS 120 ± 47; LV n.d. vorticity: sham 57 ± 5, PAS 78 ± 15 p < 0.01) despite the PAS group having normal heart rate, ejection fraction and end-diastolic volume. The intervention group demonstrated increased ejection fraction that resulted in more efficient ventricular flow compared to untreated PAS (RV n.d. vorticity: 59 ± 12 p < 0.01; LV n.d. vorticity: 41 ± 7 p < 0.001).ConclusionThese results describe previously unknown consequences of PAS on ventricular function in an animal model of unilateral PA stenosis and show that PA stent interventions improve ventricular flow efficiency. This study also highlights the sensitivity of 4D flow CMR biomarkers to detect earlier ventricular dysfunction assisting in identification of patients who may benefit from PAS interventions.

Studies of the effects of hypothermia on regional myocardial blood flow and metabolism during cardiopulmonary bypass: I. The adequately perfused beating, fibrillating, and arrested heart

Left ventricular flow dynamics and energetics derived from 4D flow CMR in patients with low gradient severe aortic stenosis

Left ventricular flow from apex to base during systole and isovolumic relaxation in a patient with hypertrophic cardiomyopathy and midventricular obstruction

2-D Left Ventricular Flow Estimation by Combining Speckle Tracking With Navier–Stokes-Based Regularization: An In Silico, In Vitro and In Vivo Study

Twenty-one patients without demonstrable coronary artery disease have been studied in the first 48 hours after aortic or mitral valve replacement to determine the possible contribution of abnormalities of left ventricular myocardial blood flow and oxygen consumption to the impaired cardiac performance which is sometimes evident in such patients. In the 14 patients making an uneventful recovery (group A), the mean value for left ventricular coronary blood flow (Kety-Schmidt method) in each study period was between 105.9 and 111.2 ml·min –1 ·100 g –1 , and myocardial oxygen consumption between 11.1 and 12.7 ml·min –1 ·100 g –1 , both being higher than in normal resting man. Oxygen extraction was 59 to 69%, and coronary sinus oxygen tension 23 to 29 mm Hg. Lactate extraction was normal. Five patients (group B) required pharmacologic support because of low cardiac output; all had undergone mitral valve replacement. In them, left ventricular coronary blood flow and oxygen consumption were the same as in group A; however, oxygen extraction was greater (68 to 79%), coronary sinus oxygen tension lower (22 to 24 mm Hg) and lactate extraction lower. Patients in group A who underwent mitral replacement (N = 4) had systemic and coronary hemodynamics and metabolism that were as satisfactory as those undergoing aortic replacement, except that left atrial pressure was higher in the first study period. When heart rate was increased from 100 to 128 beats/minute by pacing in five patients in group A, and in two additional patients, myocardial oxygen consumption increased significantly, but in four patients coronary blood flow failed to increase, oxygen extraction increased, and coronary sinus oxygen levels decreased. We conclude that in patients such as those we studied, low cardiac output postoperatively is not the result of low total left ventricular coronary blood flow or myocardial oxygen supply, but may occur in some of these patients at this time from low or absent coronary reserve and added stresses such as those from tachycardia may be met only with the potentially detrimental mechanism of increasing oxygen extraction and reducing coronary venous and myocardial oxygen levels.