Yacov Berlatzky

Perioperative Myocardial Ischemia in Carotid Endarterectomy Under Cervical Plexus Block and Prophylactic Nitroglycerin Infusion

Perioperative myocardial ischemia was evaluated in 36 consecutive carotid endarterectomy procedures carried out on patients with a high (72.2%) prevalence of ischemic heart disease. The procedures were performed under cervical plexus block plus a prophylactic intravenous nitroglycerin infusion. Findings of myocardial ischemia on perioperative (48 hours) continuous electrocardiogram recordings were correlated with preoperative cardiac status, perioperative continuous intra-arterial blood pressure measurements, and postoperative cardiac outcome. In two patients, ST segment analysis was un-interpretable because of bundle-branch blocks. Altogether, 64 episodes of significant ST segment depression were detected in 18 (52.9%) of the remaining procedures. In 8 (23.5%) procedures, ST segment depressions occurred either during carotid artery clamping at the time of the largest rise in blood pressure or within 2 hours of declamping, when blood pressure tended to decline. There were four (11.7%) postoperative cardiac events: three myocardial infarctions (one Q wave and two non-Q wave) and one episode of unstable angina pectoris. All four patients with cardiac events had early signs of myocardial ischemia either at the time of cross-clamping, or soon after declamping of the carotid artery. All myocardial infarctions developed following prolonged (> 10 hours) myocardial ischemia, starting with the first 20 hours after surgery. Thus, ST segment depression occurring during clamping or soon after carotid declamping was associated with cardiac complications (sensitivity 100% and specificity 86.6%) and suggests the possible usefulness of on-line ST segment trend monitoring.

Step baroreflex response in awake patients undergoing carotid surgery: time- and frequency-domain analysis

Step baroreceptor stimulation can provide an insight into the baroreflex control mechanism, yet this has never been done in humans. During carotid surgery under regional anesthesia, a step increase in baroreceptor stimulation occurs at carotid declamping immediately after removal of the intra-arterial atheromatous plaque. In 10 patients, the R-R interval and systolic and diastolic blood pressures (BP) were continuously recorded, and signals obtained within the time window from 10 min before until 10 min after carotid declamping were analyzed. Mean +/- SD time signals, power spectra, and transfer and coherence functions before and after declamping were calculated. Immediately after carotid declamping, both heart rate (HR) and BP declined in an exponential-like manner lasting 10.3 +/- 5.9 min, and their power spectra increased in the entire frequency range. Transfer function magnitude and coherence functions between BP and HR increased predominantly in the midfrequency region (approximately 0.1 Hz), with no change in phase function. Thus, in carotid endarterectomy patients, step increase in baroreceptor gain elicits a prolonged decline in HR and BP. Frequency analyses support the notion that the baroreflex control mechanism generates the midfrequency HR and BP variability, although other frequency regions are also affected.Step baroreceptor stimulation can provide an insight into the baroreflex control mechanism, yet this has never been done in humans. During carotid surgery under regional anesthesia, a step increase in baroreceptor stimulation occurs at carotid declamping immediately after removal of the intra-arterial atheromatous plaque. In 10 patients, the R-R interval and systolic and diastolic blood pressures (BP) were continuously recorded, and signals obtained within the time window from 10 min before until 10 min after carotid declamping were analyzed. Mean ± SD time signals, power spectra, and transfer and coherence functions before and after declamping were calculated. Immediately after carotid declamping, both heart rate (HR) and BP declined in an exponential-like manner lasting 10.3 ± 5.9 min, and their power spectra increased in the entire frequency range. Transfer function magnitude and coherence functions between BP and HR increased predominantly in the midfrequency region (∼0.1 Hz), with no change in phase function. Thus, in carotid endarterectomy patients, step increase in baroreceptor gain elicits a prolonged decline in HR and BP. Frequency analyses support the notion that the baroreflex control mechanism generates the midfrequency HR and BP variability, although other frequency regions are also affected.

Low-level laser irradiation inhibits abdominal aortic aneurysm progression in apolipoprotein E-deficient mice

AIMSnIncreased early detection of abdominal aortic aneurysm (AAA) and the severe complications of its current treatment have emphasized the need for alternative therapeutic strategies that target pathogenetic mechanisms of progression and rupture. Recent in vitro studies from our laboratory have shown that low-level laser irradiation (LLLI) (780 nm) modifies cellular processes fundamental to aneurysm progression. The present study was designed to determine whether LLLI retards the progression of suprarenal AAA in vivo.nnnMETHODS AND RESULTSnHigh-frequency ultrasonography (0.01 mm resolution) was used to quantify the effect of LLLI on aneurysmatic aortic dilatation from baseline to 4 weeks after subcutaneous infusion of angiotensin II by osmotic minipumps in the apolipoprotein E-deficient mouse. At 4 weeks, seven of 15 non-irradiated, but none of the 13 LLLI, mice had aneurysmal dilatation in the suprarenal aneurysm-prone segments that had progressed to >or=50% increase in maximal cross-sectional diameter (CSD) over baseline (P = 0.005 by Fishers exact test). The mean CSD of the suprarenal segments (normalized individually to inter-renal control segments) was also significantly lower in irradiated animals (LLLI vs. non-irradiated: 1.32 +/- 0.14 vs. 1.82 +/- 0.39, P = 0.0002 by unpaired, two-tailed t-test) with a 94% reduction in CSD at 4 weeks compared with baseline. M-mode ultrasound data showed that reduced radial wall velocity seen in non-treated was significantly attenuated in the LLLI mice, suggesting a substantial effect on arterial wall elasticity.nnnCONCLUSIONnThese in vivo studies, together with previous in vitro studies from this laboratory, appear to provide strong evidence in support of a role for LLLI in the attenuation of aneurysm progression. Further studies in large animals would appear to be the next step towards testing the applicability of this technology to the human interventional setting.

Urgent endovascular stent-graft placement for traumatic penetrating subclavian artery injuries

Penetrating injuries may infrequently cause pseudoaneurysms, lacerations and arteriovenous fistulas involving the subclavian artery. These injuries present with life-threatening bleedings, associated regional injuries and critical limb ischemia and although surgery has been considered the treatment of choice, subclavian injuries pose a real surgical challenge. We prospectively examined data of six patients presenting with penetrating subclavian artery injuries that were treated by urgent endovascular stent-graft placements. All stent-grafts were deployed successfully achieving complete exclusion of the pseudoaneurysm, control of bleeding and reconstruction of the injured artery. No procedural complications, stent thrombosis or stent infections occurred during hospitalization. One patient developed stenosis at 7 months, which required angioplasty. The series mean clinical and ultrasound-CTA follow-up is 38+/-19.7 months (range 11-60 months) and 28+/-19.1 months (range 6-58 months), respectively. This series shows the feasibility of endovascular repair by means of stent-grafts for selected patients with acute penetrating injuries of the subclavian arteries. This approach proved to be safe and effective in restoring the arterial lumen and patency, excluding the pseudoaneurysms and controlling the bleeding caused by subclavian lacerations. Mid-term follow-up on stent-graft patency rates are encouraging.

Computer assisted physiologic monitoring and stability assessment in vascular surgical patients undergoing general anesthesia--preliminary data.

Background.Physiologic monitors present an influx of numerical data that can be overwhelming to the clinician. We combined several parameters in an effort to reduce the amount of information that must be continuously monitored including oxyhemoglobin saturation by pulse oximetry, end-tidal CO2 concentration, arterial blood pressure, and heart rate into an integrated measure – the health stability magnitude (HSM). The HSM is computed for a pre-determined basal period, the reference HSM (RHSM), and recalculated continuously for comparison with the baseline value. In this study we present the HSM concept and examine changes in the HSM during abdominal aortic aneurysm surgery. Materials and methods.After IRB approval, nine patients were studied. The anesthesiologist recorded all significant intra-operative events. Within a defined time interval, data were recorded and used to calculate a combined parameter, the HSM. The baseline or reference value of this index (RHSM) was calculated after the induction of anesthesia. Individual HSM values were repeatedly calculated for ten second periods after the RHSM value was established. A > 30% deviation of the HSM from the RHSM was considered significant. Deviations in the HSM were compared with events recorded by the anesthesiologist on a paper record and with there cord from an electronic record-keeping system. The deviation observed between two consecutive HSMs, called dHSM, was plotted against HSM to construct a contour diagram of data from all patients to which individual cases could be compared. Results.The plot showed that dHSM vs. HSM values were tightly clustered. The inner contour on the distribution plot contained 90% of values. Individual patient’s time course, projected on this diagram, revealed deviations form “normal” physiology. Fifty-nine events led to > 30% deviations in the HSM; 27 were anticipated events and 32 were unanticipated. Conclusion.The correlation between HSM and dHSM depicts changes in multiple monitored parameters that can beviewed using a single graphical representation. Projection of individual cases on the contour diagram may help the clinician to distinguish relative intraoperative stability from important events. Data reduction in this manner may guide clinical decision-making in response to unanticipated or unrecognized events.

Low level laser arrests abdominal aortic aneurysm by collagen matrix reinforcement in apolipoprotein E‐deficient mice

Recent in vitro studies by our group indicated that low level laser irradiation (LLLI) modifies cellular processes essential to the progression of abdominal aortic aneurysm (AAA). Using high‐frequency ultrasonography (HF‐u/s) in the angiotensin‐II (Ang‐II)‐infused, apolipoprotein‐E‐deficient (Apo‐E−/−) mouse model of AAA, we found that LLLI markedly inhibited aneurysm formation and preserved arterial wall elasticity. We now report, using quantitative histopathology, the likely mechanism underlying the preventative effect of LLLI on aneurysm formation in this model.

Inadequate reinforcement of transmedial disruptions at branch points subtends aortic aneurysm formation in apolipoprotein-E-deficient mice

INTRODUCTIONnInfusion of angiotensin-II (Ang-II) in apolipoprotein-E-deficient mice (Apo-E(-/-)) results in suprarenal abdominal aortic aneurysm (AAA) in 30-85% of cases. This study identifies the apparent mechanism by which some animals do, but others do not, develop AAA in this model.nnnMETHODSnMale Apo-E(-/-) mice were infused with Ang-II (n=21) or saline (n=6) and sacrificed at 4 weeks. Aortas were excised, embedded in paraffin, sectioned (250 μm intervals), and stained. Sites of transmedial disruption (TMD) were identified and characterized, and their relationship to the 4 major aortic side branches (celiac, superior mesenteric, and renals) were determined.nnnRESULTSnThe frequency of TMDs in Ang-II-infused mice that formed AAA (n=9) was similar to those that did not (n=12) (AAA vs. no-AAA: 25 of 36[69%] vs. 28 of 48[58%] branches, P=.3 by chi-square). All TMDs were at branch points. However, in animals with AAA, the mean maximum length of the TMDs was significantly larger (1.94±1.6 vs. 0.65±0.5mm, P=.007 by Mann Whitney U test), the #mac-2(+) macrophages per 0.01mm(2) of defect area was greater (32±10 vs. 19±11, P<.02 by Kruskal-Wallis with Conover-Inman post hoc), the % area of attempted repair occupied by collagen was less (17±13% vs. 44±15%, P=.0009 by Mann Whitney U test), and the density of collagen per unit length of media missing was also markedly less (0.13±0.2 vs. 1.14±1.0, P=.0001 by Mann Whitney U test).nnnCONCLUSIONSnReinforcement of transmedial defects at branch points by wall matrix is a key intrinsic player in limiting AAA formation in the Ang-II-infused, Apo E(-/-) mouse and a potentially important mechanism-based therapeutic target for management of small, slowly progressing aneurysms.