Sundt, Thoralf M.

Background— Preoperative factors associated with increased mortality and worse outcome after tricuspid valve replacement in patients with severe tricuspid regurgitation are poorly understood. Methods and Results— We retrospectively analyzed 189 patients (37% men; age, 67.5±11.3 years) who underwent tricuspid valve replacement for severe tricuspid regurgitation. Operative mortality rate was 10%, and was associated with intra-aortic balloon pump (odds ratio, 3.2; 95% confidence interval, 1.9 to 5.6; P <0.0001) or the presence of severe symptoms (New York Heart Association class IV relative to classes II and/or III) at the time of surgery (1.7; 95% confidence interval, 1.05 to 2.8; P =0.02). At the end of follow-up (29.3±27.1 months), 70 patients (37%) died, 6 (3%) needed tricuspid reoperation, and 41 (21.7%) were readmitted for heart failure. Seventy-eight patients (41.3%) were free from cardiovascular events (death, tricuspid reoperation, or heart failure admissions). The only echocardiographic parameter independently associated with adverse outcomes was a decrease in the right index of myocardial performance ratio. All-cause mortality was independently associated with a higher Charlson index (hazard ratio, 1.18; 95% confidence interval, 1.01 to 1.36; P =0.03), shorter right index of myocardial performance ratio (0.91; 95% confidence interval, 0.87 to 0.96; P =0.005), and preoperative New York Heart Association IV class (1.71; 95% confidence interval, 1.3 to 2.2; P <0.0001). In 68 patients with isolated tricuspid valve replacement, the associations between short right index of myocardial performance ratio, high Charlson index, New York Heart Association class IV, and increased mortality remained significant. Conclusions— Tricuspid valve replacement for severe tricuspid regurgitation can be performed with an acceptable operative mortality if patients undergo surgery before the onset of advanced heart failure symptoms. Late mortality is associated with a high preoperative Charlson index, short right index of myocardial performance ratio, and advanced New York Heart Association class.

Abstract Perturbations in cerebral hemodynamics at the time of ablation of an arteriovenous shunt have been regarded as important in the pathogenesis of swelling and hemorrhage complicating resection of arteriovenous malformations (AVMs). A carotid-jugular fistula model in the rat had previously been investigated and found to simulate in part the nonhemorrhagic pathophysiology of a large cerebral arteriovenous fistula. Utilizing this model and measuring cerebral blood flow in 14 regions with a [14C]iodoantipyrine autoradiographic technique, the effects of hypocapnea on the cerebral circulation in opened and closed fistulas were investigated. Regional cerebral blood flow (rCBF) in control animals ranged from a median of 53 to 64 ml/100 g/min at a partial arterial carbon dioxide pressure (PaCO2) of 28 ± 2 mm Hg and 85 to 112 ml/100 g/min at a PaCO2 of 40 ± 5 mm Hg. In animals with an open carotid-jugular fistula created 12 weeks before the study, these median rCBF values at comparable PaCO2 levels ranged, respectively, from 15 to 39 ml/100 g/min and 50 to 68 ml/100 g/min (the 25th percentile for the open fistula in the hypocapneic group was 15 ml/100 g/min in 5 of the 14 regions studied). In contrast, median rCBF in the closed fistula group ranged from 73 to 100 ml/100 g/min in hypocapneic animals and from 118 to 187 ml/100 g/min in normocapneic animals. These results demonstrate the preservation of CO2 reactivity; hypoperfusion in the presence of a carotid-jugular fistula, hyperemia on fistula occlusion, and the potential to induce cerebral ischemia with hyperventilation in this model of a cerebral arteriovenous fistula. These data caution against the use of hyperventilation during surgery in patients with cerebral arteriovenous malformations.

Abstract The management of the case of a 9-year-old boy with progressive cognitive impairment due to arteriovenous fistulae at the apex of the inferior sagittal sinus is reported. This represents a unique location for an extraparenchymal deep central arteriovenous malformation. The patient underwent staged ablation of the lesion by surgery. The postoperative course was complicated by expansion of an aneurysmal vein of Galen undergoing thrombosis and hyperperfusion syndrome, but the patient ultimately made a satisfactory recovery.

Abstract Three cases of large cerebral arteriovenous fistulae are presented in which surgical ablation was complicated by brain swelling from hyperperfusion breakthrough believed to be caused by acute intraoperative hypoperfusion superimposed on chronic preoperative hypoperfusion. On the basis of these cases, experimental data, and theoretical considerations, we seriously question the wisdom of using staged surgical resection of cerebral arteriovenous malformation to prevent complications related to alterations in cerebral hemodynamics. The reasons for this concern are: the repeated occurrence of acute-on-chronic hypoperfusion during staged resection; a lack of understanding of the time course for the correction of a disordered autoregulation; risk of hemorrhage between the initial and final resection; difficulty in assessing and substantiating flow reduction after subtotal resection; the rapidity of collateralization; the divergence of flow from large, readily accessible feeding arteries to deep penetrating vessels; and attenuation of the wall thickness in collateral vessels as a consequence of increased flow.

We report that regional CBF determined by the initial slope technique using 133 Xe and 85 Kr in cats and rabbits can be significantly influenced by the size of the field of measurement. The clearance curves of umbelliferone, a lipid-soluble intracellular pH fluorescent indicator, from a visually avascular 80-fm field were used to cross-correlate rCBF with focal cortical perfusion. Our findings indicate that in the cat, as the gamma or beta detector's field of volume was reduced, regional CBF (rCBF) measured by intraarterially injected 133 Xe or 85 Kr decreased in value by 33% and 28%, respectively, and the slope of the rCBF-P a co 2 response curve became less steep by 56% and 45%, respectively. Umbelliferone, measuring a much smaller volume of tissue, showed a lower normocapnic flow and a more oblique P a co 2 response curve. In the rabbits studied, the normocarbic rCBFs and the rCBF-P a co 2 response curves measured with the three techniques corresponded to those measured in the cat. These results suggest that large field/volume measurements assess a measure of flow that is a weighted average of several distinct flow compartments and that these compartments differ in their response to changes in P a co 2 .

The effects of the novel dihydronaphthyridine Ca 2+ antagonist CI-951 on focal cerebral ischemia were assessed during MCA occlusion in 30 white New Zealand rabbits under 1.0% halothane anesthesia. In vivo brain pH i and focal CBF were measured with umbelliferone fluorescense. Baseline normocapnic brain pH i and CBF were 7.02 ± 0.02 and 48.4 ± 2.9 ml/100 g/min, respectively. In the severe ischemic regions, 15 min postocclusion brain pH i , and CBF were 6.62 ± 0.04 and 14.4 ± 0.7 ml/100 g/min in controls vs. 6.60 ± 0.02 and 12.9 ± 2.3 ml/100 g/min, respectively, in animals destined to receive CI-951. Twenty minutes after MCA occlusion, CI-951 was administered at 0.5 μg/kg/min and brain pH i and CBF were determined in both regions of severe and moderate ischemia for 4 h postocclusion. Control severe ischemic sites demonstrated no significant improvement in brain pH i and only mild increases in CBF over the next 4 h. CI-951 caused significant improvement in both of these parameters. Postocclusion 4 h brain pH i and CBF measured 6.69 ± 0.04 and 18.5 ± 3.2 ml/100 g/min in controls vs. 7.01 ± 0.04 and 41.7 ± 5.3 ml/100 g/min, respectively, in CI-951 animals ( p < 0.001). Similar improvements were observed in moderate ischemic sites. In animals that demonstrated postocclusion EEG attenuation, 75% of CI-951 animals had EEG recovery as compared to 18% in controls. CI-951 may be a useful therapeutic agent for focal cerebral ischemia if histological and outcome studies verify these data.

The effects of severe hypoglycemia on brain pH, cerebral blood flow (CBF), and other physiologic and metabolic parameters were studied in 26 cats subjected to insulin hypoglycemia. Two groups were utilized to compare the effects of anesthesia. The halothane group was composed of 14 animals and the barbiturate group contained 12 animals. Insulin was administered by both the intravenous and intramuscular routes until there was a severe electroencephalographic (EEG) change or until 6 h had elapsed. The cerebral responses to hypoglycemia demonstrated the following: CBF was unaffected by severe hypoglycemia in normotensive animals with or without EEG changes; brain pH was essentially constant in all groups regardless of glucose levels, CBF, or EEG; and the EEG abnormalities corresponded closely to brain glucose levels. Cerebral adenosine triphosphate and phosphocreatine levels were lowest in the animals with isoelectric EEGs. We conclude that CBF and brain pH in the normotensive cat under general anesthesia are relatively unaffected by insulin hypoglycemia despite the presence of severe EEG changes and cerebral energy reserves. The study suggests that the P a co 2 –CBF response curve is not dependent upon the metabolic integrity of cerebral tissue and is mediated by pathways separate from those of autoregulation.

Intracellular brain pH and indicator tissue perfusion were measured with a lipid-soluble, pH-sensitive fluorescent indicator in 10 rabbits who had either severe or moderate focal ischemia depending on whether the middle cerebral artery was occluded at its main trunk or bifurcation. Preocclusion tissue indicator perfusion was 50.1 ml/100 g/min and intracellular brain pH was 7.03. In severe focal ischemia, immediate postocclusion tissue perfusion was 12.7 ml/100 g/min and intracellular brain pH was 6.64. Four hours after occlusion, the perfusion was 5.2 ml/100 g/min and intracellular brain pH was 6.08. There was EEG and histological confirmation of infarction. In the moderate focal ischemia group, immediate postocclusion flow was 20.0 ml/100 g/min and intracellular brain pH was 6.92. At 3 h, postocclusion tissue perfusion was 22.6 ml/100 g/min and intracellular brain pH was 6.86. Therefore, for the first 3 h, this ischemic penumbra was stable. At the fourth hour, both cerebral tissue perfusion and intracellular brain pH worsened. This suggests that the ischemic penumbra is a dynamic state. The rabbit is a good experimental model for the production of both severe and moderate focal ischemia.

Intracellular brain pH was measured with a lipid-soluble, pH-sensitive fluorescent indicator in 16 squirrel monkeys. Eight of these were under halothane anesthesia and eight under barbiturate anesthesia. Measurements were taken before, during, and after focal incomplete ischemia. Brain pH following 3 h of cerebral focal ischemia changed from a normal value of 7.0 to 6.5 and 6.2 in animals studied under barbiturate and halothane anesthesia, respectively. Brain pH returned toward normal after flow was restored in animals under barbiturate anesthesia but continued to deteriorate in animals under halothane anesthesia.