A 17-year-old adolescent with severe multisystem inflammatory syndrome in children (MIS-C) associated with coronavirus disease-2019 developed reduced left ventricular function and left ventricular thrombus. With treatment, his condition improved and the thrombus was dissolved. This case illustrates the risk of severe intra-cardiac thrombotic complications in patients with MIS-C.

Communications between the pulmonary artery and left atrium cause cyanosis. The images document serial haemodynamic changes in such a fistula from fetal life to the postnatal period with a successful transcatheter intervention.

A theoretical study of an unsteady two-layered blood flow through a stenosed artery is presented in this article. The geometry of a rigid stenosed artery is assumed to be $w$-shaped. The flow regime is assumed to be laminar, unsteady and uni-directional. The characteristics of blood are modelled by the generalized Oldroyd-B non-Newtonian fluid model in the core region and a Newtonian fluid model in the periphery region. The governing partial differential equations are derived for each region by using mass and momentum conservation equations. In order to facilitate numerical solutions, the derived differential equations are nondimensionalized. A well-tested explicit finite-difference method (FDM) which is forward in time and central in space is employed for the solution of a nonlinear initial boundary value problem corresponding to each region. Validation of the FDM computations is achieved with a variational finite element method algorithm. The influences of the emerging geometric and rheological parameters on axial velocity, resistance impedance and wall shear stress are displayed graphically. The instantaneous patterns of streamlines are also presented to illustrate the global behaviour of the blood flow. The simulations are relevant to haemodynamics of small blood vessels and capillary transport, wherein rheological effects are dominant.

A 4.5-year-old child with severe idiopathic pulmonary arterial hypertension underwent right-heart catheterisation, showing suprasystemic pulmonary pressure and a tiny patent ductus arteriosus with trivial right-to-left shunting. The ductus arteriosus was successfully stented with a bare metal stent. At 1-year follow-up, a remarkable improvement was observed in clinical status, functional capacity, and serology. Echocardiography confirmed a favourable cardiac remodelling.

Overconsumption of sugar-sweetened beverages has been implicated in the pathogenesis of CVD. The objective of the present study was to elucidate acute haemodynamic and microcirculatory responses to the ingestion of sugary drinks made from sucrose, glucose or fructose at concentrations similar to those often found in commercial soft drinks. In a randomised cross-over study design, twelve young healthy human subjects (seven men) ingested 500 ml tap water in which was dissolved 60 g of either sucrose, glucose or fructose, or an amount of fructose equivalent to that present in sucrose (i.e. 30 g fructose). Continuous cardiovascular monitoring was performed for 30 min before and at 60 min after ingestion of sugary drinks, and measurements included beat-to-beat blood pressure (BP) and impedance cardiography. Additionally, microvascular endothelial function testing was performed after iontophoresis of acetylcholine and sodium nitroprusside using laser Doppler flowmetry. Ingestion of fructose (60 or 30 g) increased diastolic and mean BP to a greater extent than the ingestion of 60 g of either glucose or sucrose (P< 0·05). Ingestion of sucrose and glucose increased cardiac output (CO; P< 0·05), index of contractility (P< 0·05) and stroke volume (P< 0·05), but reduced total peripheral resistance (TPR; P< 0·05), which contrasts with the tendency of fructose (60 and 30 g) to increase resistance. Microvascular endothelial function did not differ in response to the ingestion of various sugary drinks. In conclusion, ingestion of fructose, but not sucrose, increases BP in healthy human subjects. Although sucrose comprises glucose and fructose, its changes in TPR and CO are more related to glucose than to fructose.

In this work we propose a method for analysis of postsurgical haemodynamics after femoralartery treatment of occlusive vascular disease. Patient specific reconstruction algorithmof 1D core network based on MRI data is proposed as a tool for such analysis. Along withpresurgical ultrasound data fitting it provides effective personalizing predictive methodthat is validated with clinical observations.

Pulmonary arteriovenous malformations in patients with congenital heart disease have been associated with interruption of hepatic venous return to the lungs. We report a novel technique to improve systemic saturation using a modified covered stent in a patient with unilateral left pulmonary arteriovenous malformations in the setting of a Fontan circulation.

Background: We performed a genome-wide scan in a homogeneous Arab population to identify genomic regions linked to blood pressure (BP) and its intermediate phenotypes during mental and physical stress tests. Methods: The Oman Family Study subjects (N = 1277) were recruited from five extended families of ~10 generations. Hemodynamic phenotypes were computed from beat-to-beat BP, electrocardiography and impedance cardiography. Multi-point linkage was performed for resting, mental (word conflict test, WCT) and cold pressor (CPT) stress and their reactivity scores (s), using variance components decomposition-based methods implemented in SOLAR. Results: Genome-wide scans for BP phenotypes identified quantitative trait loci (QTLs) with significant evidence of linkage on chromosomes 1 and 12 for WCT-linked cardiac output (LOD = 3.1) and systolic BP (LOD = 3.5). Evidence for suggestive linkage for WCT was found on chromosomes 3, 17 and 1 for heart rate (LOD = 2.3), DBP (LOD = 2.4) and left ventricular ejection time (LVET), respectively. For △WCT, suggestive QTLs were detected for CO on chr11 (LOD = 2.5), LVET on chr3 (LOD = 2.0) and EDI on chr9 (LOD = 2.1). For CPT, suggestive QTLs for HR and LVET shared the same region on chr22 (LOD 2.3 and 2.8, respectively) and on chr9 (LOD = 2.3) for SBP, chr7 (LOD = 2.4) for SV and chr19 (LOD = 2.6) for CO. For △CPT, CO and TPR top signals were detected on chr15 and 10 (LOD; 2.40, 2.08) respectively. Conclusion: Mental stress revealed the largest number of significant and suggestive loci for normal BP reported to date. The study of BP and its intermediate phenotypes under mental and physical stress may help reveal the genes involved in the pathogenesis of essential hypertension.

Inodilators are used in the treatment of low cardiac output, mainly after cardiac surgery. At present, there is little knowledge of the effect of inodilators in the newborn heart. Immediately after birth and in the neonatal period, the metabolism and physiology of the heart undergo major changes. We hypothesised that effects of the inodilators milrinone and levosimendan on myocardial contractility and haemodynamics under normal physiological conditions were age dependent. Animal studies were conducted on 48 pigs using a closed-chest biventricular conductance catheter method. Pigs in two age groups, that is, 5–6 days and 5–6 weeks, were assigned to milrinone, levosimendan, or a control group. We observed that both milrinone – 19.2% with a p value of 0.05 – and levosimendan – 25.7% with a p value of 0.03 compared with the control group increased cardiac output, as well as myocardial contractility with a maximum pressure development over time: milrinone 28.2%, p = 0.01 and levosimendan 19.4%, p = 0.05. Milrinone improved diastolic performance (p < 0.05) in the left ventricle in the 5–6-week-old animals. In the newborn animals, neither of the inodilators increased ventricular contractility or cardiac output; however, we observed a significant decrease in the mean arterial pressure: milrinone 34.6%, p < 0.01 and levosimendan 30.1%, p = 0.02. Both inodilators demonstrated age-dependent haemodynamic effects, and it is noteworthy that neither milrinone nor levosimendan was able to increase cardiac output in the newborn heart.

Postprandial lipaemia impairs endothelial function, possibly by changes in oxidative stress, but whether this affects cardiac output and/or systemic vascular resistance (SVR) at rest and in response to dynamic exercise remains uncertain. The present study set out to investigate the effects of a high-fat meal (HFM) v. a low-fat, high-carbohydrate meal (HCM) on cardiac output and SVR. A HFM (50 g fat) and an isoenergetic HCM (5 g fat) were randomly fed to thirty healthy adults using a crossover design. Cardiac output, heart rate and blood pressure (BP) were measured, and stroke volume and SVR were calculated over a 3 h rest following the meal, during exercise 3 h postprandially and for 45 min post-exercise. Blood samples were collected at fasting, 3 h postprandially and immediately post-exercise. Plasma TAG increased by 63·8 % 3 h following the HFM, and NEFA fell by 94·1 % 3 h after the HCM. There was a 9·8 % rise in plasma 8-isoprostane-F2α concentration following the HFM, and a 6·2 % fall following the HCM. Cardiac output increased postprandially, but the difference between meals at rest or exercise was not statistically significant. The HFM resulted in a 3·2 mmHg (95 % CI 0·7, 5·7) smaller increase in exercise mean arterial BP compared with the HCM due to a greater fall in exercise SVR. Postprandial lipaemia induced by a HFM does not affect cardiac output and/or SVR at rest, but it blunts the increase in BP during exercise.

Cardiac and pulmonary physiology in patients with functionally univentricular hearts is markedly different from that found in the setting of the normal circulation. The physiology of both the heart and the lungs remains abnormal after palliative procedures, such as creation of systemic-to-pulmonary shunts, banding of the pulmonary trunk, or creation of the cavo-pulmonary connections. In this brief review, I will concentrate on two main aspects of physiology, namely oxygenation and haemodynamics. I will make comparisons between the normal circulation and the functionally univentricular circulation, the latter both before and after creation of a cavo-pulmonary connection. To finish, I will discuss the physiology of the cavo-pulmonary connection itself, and consider some clinical implications.

The recent developments in imaging techniques have created new opportunities to give an accurate description of the three-dimensional morphology of vessels. Such three-dimensional reconstruction of anatomical structures from medical images has achieved importance in several applications, such as the reconstruction of human bones, spine portions, and vascular districts.

more than 30 years ago, fontan and baudet proposed bypass of a dysfunctional right ventricle by connecting the pulmonary arteries directly to the right atrium, the so-called atriopulmonary anastomosis. since then, much experience has been accrued in the field of the functionally univentricular circulation. the proposed connections have been subjected to several modifications, aiming towards minimizing the losses of energy in the cavopulmonary system, and thereby improving the clinical outcomes. a remarkable improvement was achieved with the introduction of the concept of the total cavopulmonary connection, specifically the combination of a bi-directional glenn anastomosis with a tubular intracardiac extension from the inferior caval venous to the pulmonary arteries. this design was shown to avoid the dissipation of energy associated with the swirling patterns seen in the traditional atrio-pulmonary anastomosis.

among the operations which lead to a partial rerouting of the systemic venous return into the pulmonary arteries, the bidirectional cavopulmonary anastomosis is frequently utilised in the staged surgical management of patients with functionally univentricular hearts. whereas some surgeons insist on closing any other source of pulmonary blood flow while performing a bidirectional cavopulmonary anastomosis, others maintain patency of either a stenosed native pulmonary outflow tract, or of a systemic-to-pulmonary arterial shunt. it remains controversial as to whether an additional source of pulmonary arterial blood flow can safely and usefully be left at the time of the bidirectional cavopulmonary anastomosis to increase systemic saturation, or whether it should be eliminated to reduce the volume load on the ventricle.

Five male ponies (3–6 years, 208±11 kg) were used to examine the haemodynamic effects of resistance exercise. The experiment consisted of a 30 min catheterization period and a 15 min equilibration period followed by the test. Initially, the ponies stood quietly on a treadmill for collection of 5 min of baseline data. They then walked at 1.9 m s−1 for 1 min sets while carrying 0 kg, 67 kg or 134 kg of weight loaded on the saddle area. Weights were applied in a randomized order using a chain hoist and sling. The ponies rested unloaded for 2 min between sets and all cardiovascular parameters returned to baseline before beginning the next set. Haemodynamic measurements (heart rate (HR), carotid artery systolic (SP), diastolic (DP), pulse (PP) and mean pressure (MAP), right atrial pressure (RAP), right ventricular pressure (RVP) and right ventricular maximum rate of pressure rise (dP/dtmax)) were recorded continuously and data collected during the last 18 s of each set were averaged and analysed. HR increased (P<0.05) with unloaded exercise (201%) and with increases in load (252 and 271% at 67 and 134 kg, respectively). RAP increased (P<0.05) with exercise, with differences (P<0.05) between the response to the 0 kg (66%), 67 kg (121%) and 134 kg (138%) loads. RVP increased (P<0.05) incrementally with load during exercise (58, 110 and 136%, respectively), with differences (P<0.05) between 0 versus 67 kg and 67 versus 134 kg. Right ventricular dP/dtmax increased (P<0.05) incrementally and showed differences (P<0.05) between loads (131, 191 and 252% at 0, 67 and 134 kg, respectively). There were increases (P<0.05) in MAP (20%), SP (20%) and DP (27) with exercise, but no difference (P>0.05) between the response to 67 versus 134 kg load (43 and 51%; 40 and 46%; 49 and 62, respectively). Pulse pressure did not change (P>0.05) from baseline values. These data suggest that resistance exercise in the form of weight carried increases intraventricular pressure through a significant increase in both cardiac pre-load and after-load.

Aims: To determine the accuracy of data relating to pulmonary vascular resistance data in patients with a bidirectional Glenn anastomosis as calculated using predicted versus measured uptake of oxygen. Methods: We studied retrospectively the data from 33 patients with a bidirectional Glenn anastomosis who underwent cardiac catheterisation prior to surgery to complete the Fontan circulation. Their weight ranged from 5.4 to 51.7 kg, and they were aged up to 12 years. Uptake of oxygen was measured using the Deltatrac II metabolic monitor. From the calculated indexed pulmonary vascular resistance, cases were stratified according to the risk of failure of the subsequent Fontan circulation. The six patients with a resistance of greater than 4 Um2 were deemed at high risk, the six with a resistance from 3 to 4 Um2 at moderate risk, and the 21 patients with a resistance less than 3 Um2 at low risk. Uptake of oxygen was also estimated from the predictive formulas of Lindahl, Lundell et al. and LaFarge and Miettinen. The indexed resistance was similarly calculated using these formulas and a comparable stratification of risk made from this data. Results: The predicted values for uptake of oxygen were consistently higher than those measured, leading to an underestimation of indexed resistance, with mean difference between −0.62 and −1.57 Um2. This difference resulted in misclassification of between five and nine of the 12 patients considered at moderate or high risk as being at low-risk. No other haemodynamic data could reliably separate the subjects deemed at low-risk from those considered to be at high-risk. A transpulmonary gradient of greater than 7 mm of mercury was found to be 100 percent specific for elevated indexed resistance, but only 60 percent sensitive. Conclusions: In patients with bidirectional Glenn anastomoses, all formulas based on predictive uptake of oxygen lead to underestimation of the true indexed pulmonary vascular resistance, to an extent that could significantly influence clinical decision-making. The transpulmonary gradient is not a reliable surrogate for indexed pulmonary vascular resistance.