Animal model to compare the effects of suture technique on cross-sectional compliance on end-to-side anastomoses.

OBJECTIVE: An animal model has been developed to compare the effects of suture technique on the luminal dimensions and compliance of end-to-side vascular anastomoses. METHODS: Carotid and internal mammalian arteries (IMAs) were exposed in three pigs (90 kg). IMAs were sectioned distally to perform end-to-side anastomoses on carotid arteries. One anastomosis was performed with 7/0 polypropylene running suture. The other was performed with the automated suture delivery device (Perclose/Abbott Labs Inc.) that makes a 7/0 polypropylene interrupted suture. Four piezoelectric crystals were sutured on toe, heel and both lateral sides of each anastomosis to measure anastomotic axes. Anastomotic cross-sectional area (CSAA) was calculated with: CSAA = pi x mM/4 where m and M are the minor and major axes of the elliptical anastomosis. Cross-sectional anastomotic compliance (CSAC) was calculated as CSAC=Delta CSAA/Delta P where Delta P is the mean pulse pressure and Delta CSAA is the mean CSAA during cardiac cycle. RESULTS: We collected a total of 1200000 pressure-length data per animal. For running suture we had a mean systolic CSAA of 26.94+/-0.4 mm(2) and a mean CSAA in diastole of 26.30+/-0.5 mm(2) (mean Delta CSAA was 0.64 mm(2)). CSAC for running suture was 4.5 x 10(-6)m(2)/kPa. For interrupted suture we had a mean CSAA in systole of 21.98+/-0.2 mm(2) and a mean CSAA in diastole of 17.38+/-0.3 mm(2) (mean Delta CSAA was 4.6+/-0.1 mm(2)). CSAC for interrupted suture was 11 x 10(-6) m(2)/kPa. CONCLUSIONS: This model, even with some limitations, can be a reliable source of information improving the outcome of vascular anastomoses. The study demonstrates that suture technique has a substantial effect on cross-sectional anastomotic compliance of end-to-side anastomoses. Interrupted suture may maximise the anastomotic lumen and provides a considerably higher CSAC than continuous suture, that reduces flow turbulence, shear stress and intimal hyperplasia. The Heartflo anastomosis device is a reliable instrument that facilitates performance of interrupted suture anastomoses.

The renin-angiotensin system and arterial wall behavior.

To assess the behavior of the arterial wall in hypertensive patients, we developed a noninvasive ultrasonic device. Simultaneous recordings of internal diameter and blood pressure over the whole cardiac cycle are used to establish compliance-pressure curves. Blood pressure, which is a co-determinant of compliance, is thus taken into account. This method allows one to compare arteries from patients with different blood pressures. Arterial compliance and distensibility were first investigated in healthy young volunteers administered either lisinopril (20 mg), atenolol (100 mg) or nitrendipine (20 mg) once a day. After 8 days of treatment, only lisinopril was found to increase arterial compliance. Subsequently, we compared arterial diameter- and distensibility-pressure curves from newly diagnosed and untreated hypertensive patients with those of matched normotensive control patients. Diameter-pressure curves did not differ significantly between the groups and distensibility was not reduced. Similar findings were later obtained in an animal model, when mechanical properties of carotid arteries were compared between spontaneously hypertensive rats and normotensive counterparts (Wistar-Kyoto rats). These results, although interesting by providing noninvasive information on the elastic response of the wall, call for further development of the technique to be able to measure arterial wall thickness. Stress-strain relationship could ultimately be established to thoroughly characterize physical properties of blood vessel walls.

Severe hypertension and massive proteinuria in a newborn with renal artery stenosis.

Renal vein thrombosis and the congenital nephrotic syndrome have been associated with nephrotic-range proteinuria/nephrotic syndrome and hypertension in the newborn period. We describe a newborn with severe hypertension and proteinuria secondary to unilateral renal artery stenosis. Proteinuria completely disappeared with blood pressure control (with sodium nitroprusside and an angiotensin-converting enzyme inhibitor). Although renin was not measured, we speculate that proteinuria might have been induced by a high renin state, and was controlled by the angiotensin-converting enzyme inhibitor.

Assessment of coronary stenosis, plaque burden and remodeling by multidetector computed tomography in patients referred for suspected coronary artery disease.

Aims To compare multidetector computed tomography (MDCT) with intravascular ultrasound (IVUS) and invasive quantitative coronary angiography (QCA) for assessment of coronary lesions in patients referred for suspected coronary artery disease (CAD). Methods and results We studied 57 patients (48 men; mean age: 63 +/- 10 years) who underwent 64-slice MDCT because of atypical chest pain, stable angina, or ECG abnormalities and were diagnosed with CAD. All patients subsequently underwent QCA and IVUS. We analyzed 102 coronary lesions using the three techniques. Measurements of luminal area stenosis and cross-sectional area by MDCT (72.9 +/- 7.0% and 4.5 +/- 1.8 mm(2), respectively) were in good agreement with those by IVUS [72.7 +/- 6.7% and 4.5 +/- 1.6 mm(2), respectively; Lin's concordance correlation coefficient r = 0.847; 95% confidence interval (CI) = 0.792-0.902 and r = 0.931; 95% CI = 0.906-0.956, respectively] but not QCA (r = 0.115; 95% CI = 0.040-0.189 and r = 0.433; 95% CI = 0.291-0.576, respectively). Plaque cross-sectional area and plaque volume measured by MDCT (12.4 +/- 3.8 mm(2) and 104.7 +/- 52.8 mu l, respectively) were in good agreement with those by IVUS (12.2 +/- 3.7 mm(2) and 102.8 +/- 54.1 mu l; r = 0.913; 95% CI = 0.880-0.945 and r = 0.979; 95% CI = 0.969-0.990, respectively). Remodeling index measurements by MDCT (1.22 +/- 0.22) were in good agreement with those by IVUS (r = 0.876; 95% CI = 0.831-0.922). Positive remodeling occurred in 63% of stenoses. Conclusion MDCT allows accurate noninvasive assessment of coronary stenosis, plaque burden and remodeling in patients referred for suspected CAD. Positive remodeling is a frequent finding in stable lesions. J Cardiovasc Med 12:122-130 (C) 2011 Italian Federation of Cardiology.

Long-term outcome of congenital aortic valve stenosis: predictors of reintervention.

OBJECTIVES: To evaluate long-term outcome of initial aortic valve intervention in a paediatric population with congenital aortic stenosis, and to determine risk factors associated with reintervention. PATIENTS AND METHODS: From 1985 to 2009, 77 patients with congenital aortic stenosis and a mean age of 5.8±5.6 years at diagnosis were followed up in our institution for 14.8±9.1 years. RESULTS: First intervention was successful with 86% of patients having a residual peak aortic gradient 1 regurgitation increased by 7%. Long-term survival after the first procedure was excellent, with 91% survival at 25 years. At a mean interval of 7.6±5.3 years, 30 patients required a reintervention (39%), mainly because of a recurrent aortic stenosis. Freedom from reintervention was 97, 89, 75, 53, and 42% at 1, 10, 15, 20, and 25 years, respectively. Predictors of reintervention were residual peak aortic gradient (p=0.0001), aortic regurgitation post-intervention >1 (p=0.02), prior balloon aortic valvuloplasty (p=0.04), and increased left ventricular posterior wall thickness (p=0.1). CONCLUSIONS: Aortic valve intervention is a safe and effective procedure for congenital aortic stenosis with excellent survival results. However, rate of reintervention is high and influenced by increased left ventricular posterior wall thickness pre-intervention, prior balloon valvuloplasty, higher residual peak systolic valve gradient, and more than mild regurgitation post-intervention. The study highlights that long-term follow-up is recommended for these patients.

Intravital microscopy reveals endothelial dysfunction in resistance arterioles in Angiotensin II-induced hypertension.

It is known that hypertension is associated with endothelial dysfunction and that Angiotensin II (Ang II) is a key player in the pathogenesis of hypertension. We aimed to elucidate whether endothelial dysfunction is a specific feature of Ang II-mediated hypertension or a common finding of hypertension, independently of underlying etiology. We studied endothelial-dependent vasorelaxation in precapillary resistance arterioles and in various large-caliber conductance arteries in wild-type mice with Ang II-dependent hypertension (2-kidney 1-clip (2K1C) model) or Ang II-independent (volume overload) hypertension (1-kidney 1-clip model (1K1C)). Normotensive sham mice were used as controls. Aortic mechanical properties were also evaluated. Intravital microscopy of precapillary arterioles revealed a significantly impaired endothelium-dependent vasorelaxation in 2K1C mice compared with sham mice, as quantified by the ratio of acetylcholine (ACh)-induced over S-nitroso-N-acetyl-D,L-penicillamine (SNAP)-induced vasorelaxation (2K1C: 0.49±0.12 vs. sham: 0.87±0.11, P=0.018). In contrast, the ACh/SNAP ratio in volume-overload hypertension 1K1C mice was not significantly different from sham mice, indicating no specific endothelial dysfunction (1K1C: 0.77±0.27 vs. sham: 0.87±0.11, P=0.138). Mechanical aortic wall properties and endothelium-dependent vasorelaxation, assessed ex vivo in rings of large-caliber conductance (abdominal and thoracic aorta, carotid and femoral arteries), were not different between 2K1C, 1K1C and sham mice. Endothelial dysfunction is an early feature of Ang II- but not volume-overload-mediated hypertension. This occurs exclusively at the level of precapillary arterioles and not in conduit arteries. Our findings, if confirmed in clinical studies, will provide a better understanding of the pathophysiological mechanisms of hypertension.

Neuro-ophthalmic emergencies for the neurologist.

A variety of acute neurologic disorders present with visual signs and symptoms. In this review the authors focus on those disorders in which the clinical outcome is dependent on timely and accurate diagnosis. The first section deals with acute visual loss, specifically optic neuritis, ischemic optic neuropathy (ION), retinal artery occlusion, and homonymous hemianopia. The authors include a discussion of those clinical features that are helpful in distinguishing between inflammatory and ischemic optic nerve disease and between arteritic and nonarteritic ION. The second section concerns disc edema with an emphasis on the prevention of visual loss in patients with increased intracranial pressure. The third section deals with abnormal ocular motility, and includes orbital inflammatory disease, carotid-cavernous fistulas, painful ophthalmoplegia, conjugate gaze palsies, and neuromuscular junction disorders. The final section concerns pupillary abnormalities, with a particular emphasis on the dilated pupil and on carotid artery dissection. Throughout there are specific guidelines for the management of these disorders, and areas are highlighted in which there is ongoing controversy.

Anastomotic longitudinal stress due to modification of arterial longitudinal properties after anastomosis.

BACKGROUND: In our hands, in vivo segmental vessel length changes up to 5% because of blood pressure: increasing in arterial pressure is associated to decrease in segmental vessel length. METHODS AND MATERIAL: Using two piezoelectric crystals sutured on vessel wall and a high fidelity pressure probe, we recorded artery length variations as function of blood pressure, before and after an end-to-end anastomosis on four pigs carotid arteries. RESULTS: Mean arterial pressure before anastomosis = 73 mmHg (+/- 12); mean arterial pressure after anastomosis = 91 mmHg (+/- 14); mean crystals displacement before anastomosis during systole = -0.21 mm; mean crystals displacement after anastomosis during systole = +0.24 mm; mean distance between crystals before anastomosis = 12.3 mm (+/- 0.8) and after anastomosis = 11.2 mm (+/- 0.5). CONCLUSIONS: In the acute phase following an end-to-end anastomosis, an increase in blood pressure causes increasing in vessel length, with an exponential correlation. The anastomosis is constantly subjected to a longitudinal traction whose magnitude depends on blood pressure.

Block of the superior cervical ganglion, description of a novel ultrasound-guided technique in human cadavers.

OBJECTIVE.: Injection of opioids to the superior cervical ganglion (SCG) has been reported to provide pain relief in patients suffering from different kinds of neuropathic facial pain conditions, such as trigeminal neuralgia, postherpetic neuralgia, and atypical facial pain. The classic approach to the SCG is a transoral technique using a so-called "stopper" to prevent accidental carotid artery puncture. The main disadvantage of this technique is that the needle tip is positioned distant from the actual target, possibly impeding successful block of the SCG. A further limitation is that injection of local anesthetics due to potential carotid artery puncture is contraindicated. We hypothesized that the SCG can be identified and blocked using ultrasound imaging, potentially increasing precision of this technique. INTERVENTIONS.: In this pilot study, 20 US-guided simulated blocks of the SCG were performed in 10 human cadavers in order to determine the accuracy of this novel block technique. After injection of 0.1 mL of dye, the cadavers were dissected to evaluate the needle position and coloring of the SCG. RESULTS.: Nineteen of the 20 needle tips were located in or next to the SCG. This corresponded to a simulated block success rate of 95% (95% confidence interval 85-100%). In 17 cases, the SCG was completely colored, and in two cases, the caudal half of the SCG was colored with dye. CONCLUSIONS.: The anatomical dissections confirmed that our ultrasound-guided approach to the SCG is accurate. Ultrasound could become an attractive alternative to the "blind" transoral technique of SCG blocks.

Structural alterations of the coronary arterial wall are associated with myocardial flow heterogeneity in type 2 diabetes mellitus.

PURPOSE: To determine the relationship between carotid intima-media thickness (IMT), coronary artery calcification (CAC), and myocardial blood flow (MBF) at rest and during vasomotor stress in type 2 diabetes mellitus (DM). METHODS: In 68 individuals, carotid IMT was measured using high-resolution vascular ultrasound, while the presence of CAC was determined with electron beam tomography (EBT). Global and regional MBF was determined in milliliters per gram per minute with (13)N-ammonia and positron emission tomography (PET) at rest, during cold pressor testing (CPT), and during adenosine (ADO) stimulation. RESULTS: There was neither a relationship between carotid IMT and CAC (r = 0.10, p = 0.32) nor between carotid IMT and coronary circulatory function in response to CPT and during ADO (r = -0.18, p = 0.25 and r = 0.10, p = 0.54, respectively). In 33 individuals, EBT detected CAC with a mean Agatston-derived calcium score of 44 +/- 18. There was a significant difference in regional MBFs between territories with and without CAC at rest and during ADO-stimulated hyperemia (0.69 +/- 0.24 vs. 0.74 +/- 0.23 and 1.82 +/- 0.50 vs. 1.95 +/- 0.51 ml/g/min; p < or = 0.05, respectively) and also during CPT in DM but less pronounced (0.81 +/- 0.24 vs. 0.83 +/- 0.23 ml/g/min; p = ns). The increase in CAC was paralleled with a progressive regional decrease in resting as well as in CPT- and ADO-related MBFs (r = -0.36, p < or = 0.014; r = -0.46, p < or = 0.007; and r = -0.33, p < or = 0.041, respectively). CONCLUSIONS: The absence of any correlation between carotid IMT and coronary circulatory function in type 2 DM suggests different features and stages of early atherosclerosis in the peripheral and coronary circulation. PET-measured MBF heterogeneity at rest and during vasomotor stress may reflect downstream fluid dynamic effects of coronary artery disease (CAD)-related early structural alterations of the arterial wall.

Influence of anatomical variations on lumbar foraminal stenosis pathogenesis.

INTRODUCTION: Symptomatic foraminal stenosis has been observed in patients with degenerative disc disease, scoliosis, asymmetrical disc degeneration and spondylolisthesis. Nevertheless not all patients with the above pathologies will develop symptomatic foraminal stenosis. We hypothesised that symptomatic patients have anatomical predisposition to foraminal stenosis, namely a larger pedicle height (PH) to vertebral body height (VH) ratio, leaving less room below the pedicle for the exiting nerve root compared to asymptomatic patients. PATIENT SAMPLE: 66 Patients were divided in two groups. The surgical group consisted of 37 patients (average age of 61 years) who presented with severe radicular symptoms resisting to conservative measures and requiring decompression and transforaminal lumbar interbody fusion (TLIF). The control group consisted of 29 patients (average age of 51 years) presenting with low back pain (LBP) but with no radicular symptoms and who were treated conservatively. METHODS: We measured VH at the level of the posterior wall as well as PH on parasagittal images (CT or MRI) on all lumbar levels (L1 to L5). Statistical analysis was performed using Student's t test. RESULTS: No difference in PH was found between the two groups for L1 to L4 levels. By contrast, there was a highly statistically significant difference in VH between the two groups from L1 to L4 level. In the surgical group, the VH was smaller (p < 0.001). CONCLUSIONS: Symptomatic patients with foraminal stenosis have smaller VH leading to lesser space beneath the pedicle and putting the exiting nerve root at risk in cases of spondylolisthesis or disc degeneration.

Neuropeptide Y infusion decreases plasma renin activity in postmyocardial infarction rats.

We wished to determine if chronic neuropeptide Y (NPY) infusion (1 ng/min for 1 week by Alzet minipump) could decrease plasma renin activity (PRA) and norepinephrine (NE) in a rat myocardial infarction (MI) model of moderate compensated congestive heart failure (CHF). CHF was produced by prior (6-8 weeks) ligation of the left coronary artery; control rats were sham-operated. Carotid arterial blood was drawn for PRA and NE in conscious unrestrained rats that had been instrumented 24 h earlier. MI rats had increased PRA as compared with sham-operated rats [8.73 +/- 1.27 vs. 5.10 +/- 0.91 ng angiotensin (AI) I/ml.h, mean +/- SE]. During chronic NPY infusion, PRA was reduced to normal in the MI group (4.78 +/- 0.91) but was not affected in the sham group (5.65 +/- 0.51). Plasma NE was altered similarly, but the changes did not reach statistical significance. These data suggest that NPY has the capacity to restrain renin release in moderate compensated CHF.

A case of dissection of intracranial cerebral arteries with segmental mediolytic "arteritis".

The intravital diagnosis of intracranial arterial dissection is not always possible due to atypic and non-specific clinical and radiological presentations. The postmortem pathological examination of cerebral blood vessels is therefore necessary to establish or confirm the presence of a dissecting aneurysm of intracranial arteries. Most of the described cases showed no significant underlying vascular pathology. Here we present the case of a 24-year-old women who died 5 days after admission to the hospital for a rapidly developing right-sided hemisyndrome. Neuroradiological examination had revealed ill-defined bifrontal hypodense lesions and angiographic findings were compatible with a dissection of the left extracranial internal carotid artery with embolic subocclusion of both anterior cerebral arteries. The pathological evaluation ruled out a thromboembolic occlusion of cerebral arteries and an extracranial internal carotid artery dissection but showed an extended dissecting process of variable age in the anterior circulation of the circle of Willis. The dissected vessels showed pathological changes characteristic of segmental mediolytic "arteritis" [Slavin and Gonzalez-Vitale 1976]. To our knowledge this is the first report on intracranial arteries being affected by this pathologic entity. Our case illustrates the importance of a postmortem examination of dissecting aneurysms of intracranial arteries. Careful serial section studies of dissected intracranial arteries in young subjects should be performed and may allow for a better understanding of the vascular pathology underlying the dissection processus.