Amount Of Collateral Flow Research Articles

Differences in Pulmonary and Systemic Flow Measurements by Cardiac Magnetic Resonance vs Cardiac Catheterization and Relation to Collateral Flow in Single Ventricle Patients.

Both cardiac magnetic resonance (CMR) and cardiac catheterization (cath) may assess patients with single ventricle physiology prior to stage II or Fontan palliation. However, development of significant aortopulmonary collaterals may invalidate assumptions of the Fick method. We compared CMR and cath flow measurements and evaluated the relation to collateral flow. This single-center study included all pre-stage II and pre-Fontan patients between 2010 and 2017 with CMR and cath within 1month. Pulmonary (Qp) and systemic flow (Qs) by cath were calculated by Fick method. CMR Qp was calculated by total pulmonary venous flow, and Qs by total vena caval flow. Collateral flow by CMR was the difference of pulmonary vein and pulmonary artery flow. In 26 studies (16 pre-stage II and 10 pre-Fontan) in 21 patients, collateral flow was higher in pre-Fontan patients (1.8 ± 0.6 vs 0.9 ± 0.8L/min/m2, p = 0.01). Overall, CMR and cath had good agreement for Qs and Qp:Qs, with moderate correlation (r = 0.44, p = 0.02 for Qs, r = 0.48, p = 0.02 for Qp:Qs). In pre-Fontan but not in pre-stage II patients, CMR had higher Qp (mean difference - 1.71L/min/m2) and Qp:Qs (mean difference - 0.36). The underestimation of cath Qp correlated with amount of collateral flow (r = - 0.47, p = 0.02). Neither cath nor CMR flow measurements correlated with outcomes in this small cohort. In conclusion, collaterals lead to systematically higher Qp and Qp:Qs measurements by CMR vs cath in single ventricle patients. Measurements may not be used interchangeably, with potential clinical significance in estimating pulmonary vascular resistance. Further study is necessary to evaluate possible relation to clinical outcomes.

Coronary wave intensity patterns in stable coronary artery disease: influence of stenosis severity and collateral circulation

ObjectiveWave intensity analysis is a method that allows separating pulse waves into components generated proximally and in the periphery of arterial trees, as well as characterising them as accelerating or...

Quantification of Systemic-to-Pulmonary Artery Collateral Flow

Abnormal vascular connections between systemic arteries and the pulmonary vascular bed—systemic-to-pulmonary collateral (SPC) vessels—manifest in patients with a variety of congenital and acquired heart disease. These vessels, which originate from branches off the brachiocephalic arteries, chest wall arteries, and the descending aorta, vary markedly in size, number, course, and distribution. Although the precise mechanisms that lead to development of SPCs are incompletely understood, hypoxemia, diminished global or regional pulmonary blood flow, and nonpulsatile flow in the pulmonary arteries are some of the commonly cited contributors.1 Indeed, SPCs are frequently encountered in patients with cardiac anomalies that include ≥1 of these abnormalities such as severe forms of tetralogy of Fallot and functional single ventricle (FSV). In the latter group, the clinical importance of SPCs and their optimal management have been topics of intense debate for >2 decades.2–6 Article see p 218 The physiology of SPC flow involves both beneficial and deleterious effects.1,2 SPCs can augment blood flow to hypoperfused lung segments, improve gas exchange, and potentially inhibit the development of pulmonary arteriovenous malformations in patients in whom hepatic venous flow does not reach the pulmonary circulation. In contrast, like other shunts, SPC flow is inherently inefficient because relatively highly oxygenated blood returns to the pulmonary circulation and potentially competes with the more efficient antegrade flow to the lungs through the native pulmonary arteries. Consequently, SPC flow results in volume load on the FSV, which can lead to ventricular dilatation and dysfunction, atrioventricular valve regurgitation, and heart failure symptoms. Other deleterious effects of excessive SPCs include flow energy loss,7 exuberant blood flow returning through the pulmonary veins to the surgical field during cardiopulmonary bypass, respiratory distress, pulmonary hypertension, and hemoptysis.8 In patients with FSV, the hemodynamic burden from SPCs has been the topic …

Impact of transverse aortic arch hypoplasia after surgical repair of aortic coarctation: An exercise echo and magnetic resonance imaging study

Background We sought to assess the impact of persistent hypoplasia of the transverse aortic arch (TAA) after repair of aortic coarctation (AoC), on blood pressure response to exercise, left ventricular (LV) hypertrophy and presence of collateral circulation. Methods 34 consecutive patients with end-to-end repair of AoC (age at repair 3.2 ± 2.5 years) underwent exercise echocardiography and magnetic resonance imaging (MRI) at 24 ± 7 years of age (range 11.3 to 44.6 years). Systolic Doppler pressure gradient (SPG) across the descending aorta and blood pressure at the right arm were measured at baseline and every minute throughout all exercise. Magnetic resonance imaging was used to measure LV mass index, presence and amount of collateral flow, and the diameters of the aortic isthmus and TAA indexed to the diameter of the diaphragmatic. Results Aortic isthmus index was higher than that of the TAA ( p = 0.006). We observed LV hypertrophy in 15 patients (45%) and presence of collateral circulation in 14 (41%). Eighteen patients (53%) had an abnormal blood pressure response to exercise. Patients with abnormal pressure response to exercise had smaller TAA index ( p = 0.0005), but similar aortic isthmus index ( p = 0.09). They also had higher exercise SPG ( p < 0.0001), higher LV mass index ( p < 0.0001) and prevalence of LV hypertrophy ( p = 0.007), higher prevalence of collateral circulation ( p < 0.0001) and a higher amount of collateral flow ( p < 0.0001). TAA index, but not aortic isthmus index, correlated with exercise blood pressure ( r = − 0.59, p = 0.003), exercise SPG ( r = − 0.70, p = 0.0005), amount of collateral flow ( r = − 0.74, p = 0.0002) and LV mass index ( r = − 0.68, p = 0.0007). Conclusions After repair of AoC, hypoplasia of the TAA may be responsible for abnormal blood pressure response to exercise, persistence of collateral circulation and LV hypertrophy.

Dynamic change in collateral flow associated with myocardial ischemia in humans

Background: This study sought to investigate how collateral flow changes during myocardial ischemia in patients. Methods: Myocardial contrast echocardiography (MCE) and rapid atrial pacing were performed in 20 patients with angiographically evidenced coronary collaterals from the right coronary artery (RCA) to the occluded left anterior descending coronary artery. Sonicated contrast medium was injected into the RCA before and immediately after atrial pacing to determine the peak background-subtracted contrast intensity (PI) in the collateral territory (PIA) and its ratio to PI in the control territory (PI ratio) as parameters of collateral blood flow. Lactate production in the coronary circulation during pacing was determined to assess myocardial ischemia in the collateral territory. Results: PIA showed a significant correlation with regional wall motion either before (r(squared)=−0.64, P<0.01) or after pacing (r(squared)=−0.65, P<0.01). Similarly, PI ratio was significantly correlated with regional wall motion either before (r(squared)=−0.54, P<0.05) or after pacing (r(squared)=−0.64, P<0.01). Rapid atrial pacing decreased both PIA and PI ratio significantly greater in patients with lactate production than in those without (PIA: −67±53 vs. −15±34%, P<0.05; PI ratio: −68±49 vs. −8.2±32%, P<0.05, respectively), while neither PIA nor PI ratio differ between the two groups of patients before pacing (PIA: 13.8±19. vs. 16.2±13.3U, P=0.75; PI ratio: 0.70±0.71 vs. 0.87±0.65, P=0.58, respectively). Conclusions: We concluded that (1) collateral flow determined by MCE was closely associated with regional cardiac function, and (2) not the amount of collateral flow at rest, but pacing-induced change of collateral flow seemed to be a determinant of regional ischemia in patients with coronary collaterals.

Direct intracoronary evidence of collateral steal in humans.

Coronary steal is defined as a fall in blood flow toward a certain vascular region in favor of another area during arteriolar vasodilatation, ie, a coronary flow velocity reserve (CFVR) <1. The purpose of this study was to determine the frequency of steal in patients with a wide range of collateral supply to a vascular area of interest and to assess whether steal is associated with the amount of collateral flow. One hundred patients 57+/-9 years old with a coronary artery stenosis to be dilated were examined with intracoronary (IC) Doppler guidewires. IC adenosine-induced CFVR<1 obtained distal to the stenosis was defined as steal. An index for collateral flow was determined by positioning the Doppler guidewire in the collateral-dependent vessel distal to the stenosis and measuring the flow velocity time integral during (Vi(occl), cm) and after (Vi(ø-occl)) balloon occlusion. Vi(occl)/Vi(ø-occl) was determined without and with intravenous adenosine (140 microg x kg(-1) x min(-1)). Coronary steal occurred in 10 of 100 patients. Patients with steal showed superior collaterals compared with those without steal: Vi(occl)/Vi(ø-occl)=0.65+/-0.24 in patients with steal versus 0.29+/-0.18 in those without steal (P=.0001). In all patients with steal, there was a reduction in collateral flow during intravenous adenosine-induced hyperemia, whereas in the majority (70%) of patients without steal, collateral flow increased or remained unchanged during hyperemia. Coronary steal assessed by intracoronary Doppler flow velocity measurements occurs in 10% of patients with a wide range of coronary collaterals to the vascular area from which blood flow is redistributed. There is a direct association between the presence of steal away from and the amount of collateral flow toward the region under investigation. Collateral flow to the vascular region studied decreases during adenosine-induced hyperemia, which indicates a mechanism of steal via the extensive collaterals.

Short-term prognosis of stroke due to occlusion of internal carotid artery based on transcranial Doppler ultrasonography.

The clinical course of stroke due to occlusion of the internal carotid artery is influenced by amount of collateral flow. We measured mean frequency shifts in the middle cerebral artery by transcranial Doppler ultrasonography to determine its prognostic value. Patients with proven extracranial occlusion of the internal carotid artery and ipsilateral hemispheral stroke were enrolled in our study. We performed transcranial Doppler ultrasonography on 31 patients within 48 hours after the stroke onset and followed up 25 patients in 28 days. At the same time, neurological examination with quantification of neurological deficit was done. We correlated values of flow frequency shifts on the side of stroke with degree of neurological deficit at the onset and at 28 days as well as the degree of clinical improvement and the value of frequency shifts. We found a negative correlation between blood flow frequency shifts in the middle cerebral artery and degree of neurological deficit at the onset (Spearman rank correlation coefficient, -0.567; p less than 0.001). We also found a positive correlation between the change of the neurological deficit during follow-up and frequency shifts at the onset (Spearman rank coefficient, 0.548; p less than 0.05). Diminished blood flow velocity (mean frequency shift) in the area of stroke is a negative prognostic factor for the degree of neurological deficit at the onset and a negative prognostic factor for possible improvement. Knowledge of hemodynamic conditions in the stroke area may help to improve therapeutic decisions.

Evaluation of factors influencing myocardial infarct size in unconscious dogs

The aim was to evaluate the factors determining myocardial infarct size in unconscious dogs. In anaesthetised open chest dogs, the left anterior descending coronary artery was occluded either by ligation or by thrombosis for different time periods (1.5 h, 4 h, 24 h), with or without reperfusion. Haemodynamic variables were recorded throughout the experiment. Radioactive microspheres (15 microns) were injected at the end of the ischaemic period to measure regional myocardial blood flow. Infarct size and area at risk were determined by the Evans blue triphenyltetrazolium staining technique followed by planimetry. Mongrel dogs of either sex (n = 16-42 per experiment), weight 18-25 kg, were used. A large interindividual variability in infarct size was observed after occlusion of the left anterior descending coronary artery at a standardised location for a well defined period. An examination of the factors responsible for this variability was carried out in order to develop a statistical model which would make it possible to predict infarct size. Using multiple regression analysis, it was found that in most protocols (except 90 min thrombosis) more than 85% of the variability in infarct size could be explained by the size of the area at risk and the amount of collateral flow. Thus, knowing the area at risk and the collateral flow, a fairly accurate prediction can be made of the size of the infarct that the dog will develop after a defined occlusion period. Furthermore, it was found that the infarct size increased with duration of occlusion, while duration of reperfusion had no effect. In the 90 min occlusion group thrombosis induced a larger final infarct than ligature. A correction for baseline variables is necessary in order to compare infarct size between experimental groups. The usefulness of this procedure is shown by an example of an experimental intervention, i.e., R 56,865, a drug with known cardioprotective effects.

Time course of myocardial necrosis.

The time course of myocardial ischemia was studied in canine myocardium by electron microscopy. Ischemia of the myocardium produces ultrastructural alterations of mitochondria, nuclei, contractile apparatus, and the SR- and T-tubular system that are accompanied by loss of glycogen and intracellular edema. These changes are more pronounced with increasing severity of ischemia, and they allow the differentiation between different stages of reversible and of irreversible injury. Reperfusion of reversibly injured tissue leads to structural recovery; reperfusion of irreversibly injured tissue produces further deterioration. On the basis of ultrastructural data, it was found that in a dog, after 45 minutes of coronary artery occlusion, subendocardial infarction was present in 20% of all animals. Transmural infarction was present in 24% of all dogs after 90 minutes of coronary artery occlusion and in 53% after 24 hours. The individual variability in the speed of development of infarction is caused by the rate of oxygen consumption at the time of occlusion and by the amount of collateral flow. Intermittent ischemia is much better tolerated than permanent ischemia of the same duration. Species differences are evident. The course of development of myocardial necrosis, therefore, depends on time, rate of oxygen consumption, collateral flow, mode of ischemia, and on the species investigated.

Determinants and protective potential of coronary arterial collaterals as assessed by an angioplasty model

Two indexes of collateral blood flow, the ratio of distal coronary occlusion pressure/aortic pressure (DCOP/Pao) and angiographic collateral class were determined during elective angioplasty in 36 patients with normal left ventricular function. The association between collateral indexes and 8 anatomic and clinical variables was assessed. A reduction in luminal diameter by ≥70% predicted angiographically demonstrable collaterals with 100% specificity and 85% sensitivity. Lesion severity (stenosis) correlated with both collateral class and DCOP/Pao: DCOP/Pao = 2.8809 −0.0729 × stenosis +0.00049 × stenosis 2. The data suggest a quantitative relation between lesion severity and collateral development beyond a threshold value of 70% stenosis. Left ventricular ejection fraction during ischemia caused by balloon occlusion (EFo) was found to be primarily determined by lesion location; however, collateral flow modified EFo significantly. For mid-left anterior descending and right coronary artery: EFo = 59 + 26 × (DCOP/Pao); for proximal left anterior descending artery: EFo = 24 + 89 × (DCOP/Pao). A model predicting the hemodynamic and clinical consequences of abrupt coronary closure based on lesion location and severity was developed. In the second study phase, this model was tested retrospectively in a different group of 23 patients who experienced coronary occlusion as a complication of angioplasty. The data of both study phases suggest that left ventricular function and clinical outcome after abrupt coronary closure are determined by an interaction between location of the coronary artery obstruction and the amount of collateral flow. Lesion severity and the extent of functional impairment resulting from abrupt coronary closure are inversely related.