Congestive heart failure due to traumatic arteriovenous fistula--two case reports

Arteriovenous fistulas are abnormal connections between the high-pressure and high-resistance arterial system and the venous system with opposite features. Due to its lower resistance, the blood preferentially flows via the fistula rather than through the capillary bed. The amount of shunt flow depends on its size and proximity to the heart. Due to the increase in circulating volume, progressive dilation develops in the whole vascular system proximal to the shunt. Cardiomegaly and venous distention may return to normal after surgical repair of this vascular abnormality. Two cases are presented of heart failure due to traumatic arteriovenous fistula, one of which was between the right renal artery and inferior vena cava and the other between the left renal artery and renal vein.     

An elephant trunk appearance—what is the diagnosis?

Coronary cameral fistula is a rare congenital cardiac abnormality. An 18‐year‐old boy presented with features of right heart volume overload. Clinical examination was suggestive of hyperdynamic circulation with continuous murmur in precordium. 2D echocardiography showed dilated right coronary artery, and 3D echocardiography added information in tracing the track of the fistula which was consistent with the diagnosis of right coronary cameral fistula draining into the right ventricle. Coronary angiograms revealed an unusually dilated right coronary artery giving the appearance of an “elephant trunk” and with a fistulous tract into the right ventricle. Considering the higher risks of surgery in such difficult cases, we performed a successful transcatheter closure of the fistula using an Amplatzer vascular plug.     

Assessing the deformation of pulmonary capillaries produced by ventilation

We used a Fourier transform method to compute from the density fluctuation of aortic blood the changes in the blood volume of pulmonary capillaries and the transit time from the capillaries to the aorta. First the time constants of a lagged normal density function capable of simulating the saline dilution through the central circulation were established. Then we decomposed the Fourier transform of the lagged normal density function to determine an attenuation for the estimation of the density fluctuation in blood leaving the capillaries. Regarding the low hematocrit blood in the capillaries as a density indicator, we deduced from the density fluctuation the percentage change of capillary volume for dogs ventilated mechanically. This change was found to range from 3.8 to 5.8% for frequencies within 6 to 20 cycles per minute. Based on this simulation and the delay time of the density fluctuation from the tracheal pressure, we estimated that the transit time for the density indicator being released from the pulmonary capillaries to the aorta was 45% of the mean transit time of the central circulation, suggesting that the releasing sites are midway of the pulmonary capillaries.     

The effects of short-term venous congestion on forearm venous volume and reactive hyperemia blood flow in human subjects

Congestive heart failure is associated with a reduction in limb venous volume at an effective venous pressure of 30 mm Hg (VV[30]). Further, an attenuated arteriolar dilation in response to a metabolic stimulus has been demonstrated. It was the purpose of this study to determine to what extent the chronic elevation in venous pressure seen in heart failure might explain these abnormalities of the limb circulation. Ten normal human volunteers were subjected to venous congestion of one arm for three hours at 70 mm Hg. A mercury-in-rubber strain gauge plethysmograph was used to measure forearm VV [30] and forearm blood flow at rest after release of five minutes of arterial occlusion (the reactive hyperemia response). Congestion reduced VV [30] 22%, resting forearm blood flow 49% and peak reactive hyperemia blood flow 25%. Thus, chronic venous congestion per se may significantly reduce limb venous volume as well as resting and reactive hyperemia blood flow.     

Effect of sodium nitroprusside and nitroglycerin on the resistance and capacitance system in cardiac surgery interventions

The whole-body arterial and venous dilating properties of nitroglycerin (NTG) and sodium nitroprusside (SNP) were investigated during extracorporeal circulation and normal circulation in patients undergoing coronary bypass surgery. SNP was found to lower preload and afterload for the time of drug administration. During extracorporeal circulation and normal circulation, an average volume of 340 ml was stored in the capacitance vessels when the mean arterial pressure was lowered for 20 mm Hg. When the reduction in preload was compensated by a volume load (blood transfusions), this resulted in a pure impedance reduction by SNP. NTG showed more complex effects. Even with the continuous infusion of NTG only a short-termed, self-limiting afterload reduction occurred during extracorporeal circulation. During normal circulation, the reduction in preload was more extensive with NTG than with SNP, an average volume of 600 ml was stored in the capacitance vessels when the mean arterial pressure was lowered for 20 mm Hg by NTG. While the volume storage by SNP was reversible after termination of the infusion, this was not the case with NTG, where the volume was stored for 1-2 hours. The volume storage by NTG became smaller with an increased filling of the capacitance system. Additionally, the venous resistance of the cardiopulmonary bypass showed different effects on the volume storage by SNP and NTG. In conclusion, the different effects of NTG and SNP cannot be explained by a single, homogenous compartment model of the peripheral circulation but by affecting two different compartments of the capacitance system.     

New type of asymptomatic congenital portosystemic shunt

Congenital extrahepatic portosystemic shunt (CEPS) is an extremely rare anomaly. In these malformations splanchnic blood bypasses the liver and drains into the systemic circulation through the inferior vena cava (IVC) or the left renal vein (LRV). Extrahepatic shunts may be divided into type 1 [end-to-side mesenterico-caval fistula with congenital absence of the portal vein (PV)] and type 2 (partial portocaval shunt caused by side-to-side mesenterico-caval fistula with normal or hypoplasic PV). Type 2 shunts typically are wholly extrahepatic between the PV or its right branch and the retrohepatic IVC. This report describes an asymptomatic case of CEPS not previously documented and not classifiable as type 1 or 2. CT revealed a normal PV with communication between the inferior mesenteric vein (IMV) and the LRV. The inferior mesenteric vein appeared tortuous, abnormally long and with a large calibre, and presented a connection with the LRV, in addition to a normal confluence into the splenic vein. Colour Doppler revealed hepatopetal normal flow in the PV and superior mesenteric vein with mild portal hypertension and an inversion of flow in the IMV directed to the LRV. Biochemical parameters showed a normal liver function without hyperammonaemia.     

Assessment of toe blood pressure is an effective screening method to identify diabetes patients with lower extremity arterial disease

The authors evaluated a screening program for lower extremity arterial disease (LEAD) in diabetic patients and focused on the value of toe blood pressure assessment. They recruited 437 subjects, ages 30-70 years (134 healthy controls, 166 type 1 and 137 type 2 diabetic patients; control [Ctr], DM1, and DM2) with no previous history of LEAD. They were enrolled in a longitudinal study with a planned follow-up of 10 years. Patients were consecutively enrolled from outpatient diabetes units of 2 university hospitals. Subjects were screened with respect to peripheral circulation by use of established noninvasive techniques. These included arm, ankle (AP), and toe (TP) blood pressure measurements; evaluation of peripheral neuropathy; and a standardized physical examination. Results from the baseline examination are presented in this report. The number of patients who presented peripheral pressures or indices below normal (< mean -2 SD for controls) was higher among diabetic patients; 24% of DM1 and 31% of DM2, as compared to 6% of Ctr, had at least 1 lower limb with a low TP, AP, toe/arm index (TI), or ankle/arm index (AI), and these subjects were mainly identified by using the toe/arm index. TI was independently and negatively associated with fasting blood glucose in both patient groups, and with smoking, age, and diabetes duration in DM1. The mean AP was higher in the DM1 and DM2 groups compared to Ctr, whereas overall TP, TI, and AI were similar in the groups. It was also shown that abnormally low TI was significantly more common than low AI among diabetics (p<0.001), and this was true for TP vs AP as well (p<0.05). It is beneficial to include assessment of toe blood pressure and toe/arm blood pressure index to detect early LEAD in diabetic patients. Ankle blood pressure and indices alone are less efficient, owing probably to medial sclerosis in diabetic patients. Up to 30% of diabetic patients with no ischemic symptoms may have signs of impaired arterial circulation.     

Effect of circulation time on plasma high density lipoprotein cholesterol in rats

The effect of circulation time on plasma high density lipoprotein cholesterol concentrations was investigated in 20 male Wistar rats injected with alcohol, stressed with lighting, or fed a high fat diet. Circulation time was measured during anaesthesia with a computerised dichromatic earpiece densitometer. Indocyanine green, 0.5% concentration and 0.05 ml volume, was injected directly into the intracardiac cavity. The densitometer was held against the right foot of the rat, where the concentration of indocyanine green was measured by a light absorption method. Circulation time was defined as the time during which indocyanine green passed from the heart to the foot. At the same time blood was collected for determining high density lipoprotein cholesterol concentration. The rats were randomly divided into three groups, and control circulation time and high density lipoprotein cholesterol concentrations were obtained. In six rats injected with 100% ethyl alcohol, 0.03 ml.100 g-1 body weight in volume, into the abdominal cavity and five rats placed under 400 Lux lighting for 48 h the increase in circulation time was inversely proportional to the increase in high density lipoprotein cholesterol concentration (r = -0.644, p less than 0.05). Of nine rats given a high fat diet containing 7.0% fat for 48 h, all showed increased high density lipoprotein cholesterol concentration, but no correlation was noted between the increases in circulation time and high density lipoprotein cholesterol (r = -0.303).(ABSTRACT TRUNCATED AT 250 WORDS)     

Congenital coronary artery fistula in an intercoronary communication between the left main and the diagonal branch of the left anterior descending coronary artery: An interesting case report

Intercoronary communication is a very rare coronary artery anomaly. It is defined as an open-ended circulation with bidirectional blood flow between two coronary arteries. Coronary artery fistulas are abnormal communications between a coronary artery and a cardiac chamber or major vessel. A 62-year-old man was admitted to our hospital with sudden development of general weakness, dizziness and a sensation of compression in his chest. At presentation his blood pressure was 80/40 mmHg and heart rate was 65 beats/min. The ECG revealed sinus rhythm and 1–2 mm ST elevation in the anterior leads. The patient was taken to the catheterization laboratory for percutaneous coronary intervention. The left main and left circumflex coronary arteries were normal. Coronary angiography showed a communication between the left main and the diagonal branch of the left anterior descending and a fistula between the intercoronary connection and the left atrium. The other coronary arteries were normal. Laboratory test results, including cardiac troponin I and creatine kinase–MB levels, were normal. The angina symptoms disappeared and the ST elevation resolved within four hours. We report an interesting case of congenital coronary artery fistula in an intercoronary communication between the left main and the diagonal branch of the left anterior descending coronary artery presenting as an acute coronary syndrome. To the best of our knowledge, this is the first case in the literature involving a coronary artery fistula in an intercoronary communication.     

Portal hypertension and blood viscosity

Previous studies, exploring the effect of blood viscosity on portal pressure in portal hypertensive humans and animal models, have shown conflicting results. In a series of studies, in portal vein constricted rats, we investigated effects of reduced blood viscosity on the hyperdynamic circulation, portal pressure, and vascular geometry. Blood was withdrawn at a rate of 0.3 mL/min for 15 minutes followed by 15 minutes of stabilization. The shed blood or Haemaccel was infused at the same rate and volume as used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance (reflecting vessel geometry) was calculated as resistance/viscosity ratio. In normal and portal hypertensive rats, acute volume replacement with Haemaccel, induced increase in systemic and splanchnic blood flows reflecting mainly changes in viscosity and not in blood vessel geometry. However, 24 hours later, in Haemaccel treated animals, an increased splanchnic arteriolar and porto-collateral vascular hindrance were observed. This indicated vasoconstriction in the porto-collateral vascular bed. The increase in portal venous inflow after acute volume restitution with Haemaccel was prevented by pretreatment with propranolol. Although, caution should be taken in extrapolating these results to humans, we would like to speculate that during a portal hypertensive-related bleeding episode: (1) volume replacement with low viscosity plasma expanders may aggravate the hyperdynamic circulation of portal hypertension. (2) Slow rate volume replacement enables hemodynamic adaptation to occur. (3) Volume replacement maybe more safe in a subject pretreated with propranolol.     

Stem cell factor is responsible for the rapid response in mature mast cell density in the acutely stressed heart

In the abdominal aortocaval (AV) fistula model of heart failure, we have shown that the acute doubling of cardiac mature mast cell (MC) density involved the maturation, but not proliferation, of a resident population of immature cardiac MCs. An increase in stem cell factor (SCF) may be responsible for this MC maturation process. Thus, the purpose of this study was to determine if: 1) myocardial SCF levels are increased following the initiation of cardiac volume overload; 2) the incubation of left ventricular (LV) tissue slices with SCF results in an increase in mature MC density; and 3) chemical degranulation of mature cardiac MCs in LV tissue slices results in an increase in SCF and mature MC density via MC chymase. Male rats with either sham or AV fistula surgery were studied at 6h and 1 and 3days post-surgery. LV slices from normal male rat hearts were incubated for 16h with media alone or media containing one of the following: 1) recombinant rat SCF (20ng/ml) to determine the effects of SCF on MC maturation; 2) the MC secretagogue compound 48/80 (20μg/ml) to determine the effects of MC degranulation on SCF levels and mature MC density; 3) media containing compound 48/80 and anti-SCF (5μg/ml) to block the effects of SCF; 4) chymase (100nM) to determine the effects of chymase on SCF; and 5) compound 48/80 and chymostatin (chymase inhibitor, 10μM) to block the effects of MC chymase. In AV fistula animals, myocardial SCF was significantly elevated above that in the sham group at 6h and 1day post fistula by 2 and 1.8 fold, respectively, and then returned to normal by 3days; this increase slightly preceded significant increases in MC density. Incubation of LV slices with SCF resulted in a doubling of mature MC density and this was concomitant with a significant decrease in the number of immature mast cells. Incubation of LV slices with compound 48/80 increased media SCF levels and mature MC density and with anti-SCF and chymostatin prevented these compound 48/80-induced increases. Incubation with chymase increased media SCF levels and mature MC density. These findings indicate that activated mature cardiac mast cells are responsible, in a paracrine fashion, for the increase in mature MC density post AV fistula by rapidly increasing SCF levels via the release of chymase.     

Blood volume changes in endotoxin shock

Injection of E. coli endotoxin in dogs promotes hemodynamic changes in circulating blood volume and blood components. Adult mongrel dogs were given endotoxin and studied for 3 hours. Red-blood-cell (RBC) volume and whole-blood volume was measured using the Cr-51 RBC labeling method. Hematocrit and RBC counts were taken at various time periods. Whole-blood volume was not found to change significantly over the test period; however, plasma volume demonstrated a significant decrease by 60 minutes with a parallel increase in RBC volume. Hematocrit increased significantly by 60 minutes and continued its rise to a 30% increase at 3 hours. Circulating RBC counts demonstrated a 26% increase. RBC precursors such as reticulocytes and normoblasts were counted using standard microscopic methods and were observed to increase after injection of endotoxin. These data suggest that the increases in hemoconcentration after administration of endotoxin are caused not only by the loss of plasma from the circulation but also by release of RBCs from blood-forming organs.     

Redistribution of blood volume in Type I diabetes

Aims/hypothesis. Impaired activity of endothelium-derived nitric oxide in Type I (insulin-dependent) diabetes mellitus will cause an increased vascular tone. Considering the lower production of nitric oxide in veins than in arteries, an impaired activity would have less vasoconstrictive effect in veins. The reported minimally changed total plasma volume in diabetes might, therefore, indicate a redistribution of blood volumes from the arterial to the venous side of the circulation. This could be more pronounced in patients with microalbuminuria. Methods. In 16 normoalbuminuric and 16 microalbuminuric Type I diabetic patients and 16 individually matched healthy control subjects, venous and arterial blood volumes, venous myogenic response and arterial distensibilities were assessed in the upper arm using an electrical bio-impedance method. Results. In diabetic patients, the venous blood volume and venous myogenic response were increased (p < 0.02 and p < 0.05, respectively), whereas the arterial blood volume did not change. Moreover, in diabetic patients the distensibility of the large arteries was decreased (p < 0.05) but increased in the total arterial bed (p < 0.05). Therefore, the distensibility of the small arteries must have been increased. No differences were found between normoalbuminuric and microalbuminuric diabetic patients. Conclusion/interpretation. The increase in venous blood volume and myogenic response and the decrease in distensibility of the large arteries in the upper arm are in agreement with the expected shift towards venous blood volume distribution in Type I diabetes with and without microalbuminuria. Furthermore, they support the haemodynamic hypothesis of the pathogenesis of diabetic microangiopathy. [Diabetologia (2001) 44: 429–432] Received: 11 September 2000 and in revised form: 27 November 2000     

Effect of experimental myocardial hypertrophy on coronary microcirculation in the rat

Effects of cardiac hypertrophy on coronary capillary density and volume have been studied in two models: systemic hypertension (1c. 2K Goldblatt model, n = 27), and volume overload (aorto-caval fistula, n = 27) compared to a control group (n = 27). Studies have been performed at 1 month, 3 and 6 months. Subendocardial and subepicardial coronary capillaries have been visualized by in injection of fluorescein-labeled dextran (FITC). The body weights were not significantly different in the three groups. The heart weight was the same in hypertensive model and fistula. Goldblatt model was associated with a high blood pressure and an increase in left ventricular wall thickness, whereas fistula was associated with a lower blood pressure and no difference in wall thickness as compared to controls. No difference in subepicardial capillary density was found in the three groups, whereas the subendocardial capillary density was decreased in the two models of cardiac hypertrophy (-25%). Capillary area and mean perimeter, were increased in fistula, due to vasodilatation, and decreased in Goldblatt model in relation to vasoconstriction.     

Subclavian stenosis presenting as progressive exertional angina pectoris

Left subclavian stenosis is an uncommon cause of exertional left arm pain. In a patient who presented with exertional chest and left arm pain in an increasing pattern, clinical evaluation disclosed a discrepancy between right and left arm blood pressure. Exercise stress testing with thallium revealed normal myocardial perfusion. Aortic arch and selective angiography revealed a high-grade proximal left subclavian stenosis. Subclavian angioplasty was performed with complete resolution of symptoms. This case demonstrates that ischemic left arm pain due to subclavian stenosis can present as accelerated angina, and highlights the importance of determining blood pressure in both arms in routine evaluation of patients at risk for atherosclerosis.     

The effect of early appearing extrasystoles on systemic and coronary circulation]

In 10 anaesthesized dwarf pigs with an open thorax the effects of extrasystoles on systemic and coronary circulation were investigated. The actual effect of an extrasystole depends on the time of its onset. Early extrasystoles hamper the cardiac blood perfusion, with decreases in the stroke volume, mean arterial pressure, coronary blood flow, and elevation of coronary resistance. Extrasystoles setting on later are of minor haemodynamic and coronarodynamic importance. The effects of bigeminy and 2:1 extrasystolia are more adverse than the consequences of extrasystoles with later onset. With cumulation of several consecutive extrasystoles also adverse the haemodynamic coronarodynamic sequelae increase, in dependence on the magnitude of the quotient coupling time /extrasystolic excitation period [ greater than 1.1], or of the quotient: duration of pre- and postextrasystolic intervals/ normal interval of heart action [ greater than 1.5]. The authors point out the importance of haemodynamic findings during early extrasystoles in ischaemic heart disease.     

Effect of terlipressin on blood volume distribution in patients with cirrhosis

BACKGROUND: Patients with cirrhosis and portal hypertension have an altered blood volume distribution and a hyperdynamic systemic circulation. Terlipressin is known to reduce portal pressure by decreasing splanchnic inflow, but its effect on the blood volume distribution is unknown. The aim of the study was to investigate changes in regional blood volume distribution and systemic haemodynamics after administration of terlipressin to patients with cirrhosis. METHODS: Blood volume distribution was determined in 13 patients with cirrhosis and portal hypertension by a dual-head gamma-camera technique and systemic haemodynamics was measured before and after intravenous administration of terlipressin (2 mg). RESULTS: Terlipressin increased the blood volume in the thorax region (+6.0%, P < 0.002) and the liver region (+12.2%, P < 0.002), whereas blood volume in the splanchnic region remained unchanged. Systemic vascular resistance (SVR) and mean arterial blood pressure increased after terlipressin (+34 and +21%, P < 0.001). The increase in liver blood volume correlated directly with the increase in SVR (r = 0.88. P < 0.001). CONCLUSIONS: Terlipressin ameliorates the hyperdynamic circulation, increases thorax and liver blood volumes, but produces no effect on the splanchnic blood volume. Besides decreasing the splanchnic inflow, terlipressin may affect portal pressure by causing vasodilatation of intrahepatic vessels.     

Ileovesical Fistula

A patient with regional enteritis presenting with symptoms of fecaluria and pneumaturia is presented. Most of the established technics such as upper gastrointestinal series, cystography, cystoscopy and colonoscopy failed to demonstrate the fistula in this patient. 14C PEG as a nonabsorbable marker was given by mouth and a seven-fold increase in the counts at the fourth hour of urine collection confirmed the presence of an ileovesical fistula. This increase in counts was not seen when 14C PEG test was repeated after closure of this fistula surgically and was also not seen in a similar disease control patient and a healthy normal volunteer. Total parenteral nutrition with intralipids, Freamine II and glucose given in a peripheral vein for 45 days failed to close this fistula.     

Pathophysiology of portal hypertension.

Portal hypertension is characterized by a pathologic increase in portal venous pressure that leads to the formation of an extensive network of portosystemic collaterals that divert a large fraction of portal blood to the systemic circulation, bypassing the liver. Experimental models have improved understanding of the pathophysiology of portal hypertension. It is now clear that an increased vascular resistance to portal blood flow is the initial factor responsible for the increase in portal pressure. This resistance is exerted along the hepatic and portal-collateral circulation and is in part modifiable by pharmacologic agents. In a latter stage, an increased portal venous blood inflow, promoted by splanchnic vasodilation, contributes to maintenance and aggravation of portal hypertension. Humoral vasodilatory agents play an important role in the splanchnic vasodilation. Several vasodilators are likely to be involved, including glucagon, prostacyclin, endotoxins, and nitric oxide. The splanchnic vasodilation is associated with a hyperkinetic systemic circulation, with reduced arterial pressure and peripheral resistance and increased cardiac output. The splanchnic circulation is probably the vascular territory in which the vasodilation is more pronounced. Therefore, splanchnic and systemic vasodilation probably share some pathophysiologic events. An expanded plasma volume is observed in all forms of portal hypertension. Expansion of plasma volume is due to renal sodium retention, which has been shown to precede the increase in cardiac output and can be prevented or reversed by sodium restriction and spironolactone. The expanded blood volume represents another mechanism that contributes to further increases in portal pressure.