Left ventricular outflow tract obstruction associated with chronic ventricular assist device support.

Favorable long-term patient outcome after insertion of a left ventricular assist device (LVAD) as a bridge to recovery or destination therapy for the treatment of end-stage cardiomyopathy is adversely affected by pathophysiologic changes affecting the heart. Alterations in the native aortic valve apparatus, specifically aortic valve cusp fusion, is an example of such a phenomenon and may especially affect patients in cases of bridge to recovery, a rare but reported event. A retrospective review of the last 33 LVAD placements at our institution was conducted, including reviews of operative reports and pathologic examinations of the native hearts. Seven hearts were found to have varying degrees of aortic valve cusp fusion after chronic LVAD support (63-1, 339 days). Five of these patients had native aortic valves, and two had bioprosthetic valves. The left ventricular outflow tracts in two patients were surgically occluded at the time of LVAD insertion. Aortic valve cusp fusion occurs in roughly 25% of patients on chronic LVAD support. This phenomenon may prove to be clinically significant by creating a potential source of emboli and infection. In addition, in the case of myocardial recovery, left ventricular outflow tract obstruction could limit parallel flow and produce suprasystemic ventricular pressures that in turn would elevate left ventricular end diastolic pressures. The latter may contribute to further myocardial injury, ultimately limiting the ability of an otherwise recovered heart to be weaned from LVAD support.

Renal artery dissection associated with Gz acceleration.

A 55-yr-old male presented with flank pain and nausea minutes after intensive aerobatic flight maneuvers. An initial diagnosis of acute appendicitis was made. Computed axial tomography and renal arteriography showed a right kidney with two renal arteries, a right upper pole infarction, and a dissection in the upper renal artery which had a more vertical trajectory than the usual main renal artery. No signs of diseases known to be associated with renal artery dissection were present. The patient recovered without residual hypertension. Heavy positive G loads may have potential to cause renal arterial injury, particularly when renal vascular anatomical variations exist. The postulated mechanism is similar to fall injuries in which the subjects landed on their feet, with inertia causing caudal renal dislodgement and stretch of the renal vessels.

Unshuntable extrahepatic portal hypertension revisited: 43 years' experience with radical esophagogastrectomy treatment of bleeding esophagogastric varices.

BACKGROUND: In 1994, the authors reported their experience with radical esophagogastrectomy for bleeding esophagogastric varices due to unshuntable extra-hepatic portal hypertension. Since then, the series has expanded from 22 to 44 patients. The aim of this study was to assess the validity of the previous observations and conclusions in the largest series with the longest follow-up. METHODS: From 1968 to 2005, 44 patients with unshuntable extra-hepatic portal hypertension were treated by total gastrectomy and resection of the distal two thirds of the esophagus. Before referral, the patients experienced 4 to 24 episodes of variceal bleeding requiring a mean 130 U of blood transfusion, 15 hospital admissions, and 6 previous unsuccessful operations. RESULTS: Transient postoperative complications occurred in 50% of patients. The survival rate is 100%, with no recurrence of variceal bleeding during 7 to 43 years of follow-up. Liver function and biopsy results have been normal. Quality of life has been excellent or good in 91%. Eighty-six percent have resumed employment or full-time housekeeping. CONCLUSIONS: In unshuntable extra-hepatic portal hypertension, radical esophagogastrectomy is the only consistently effective treatment of variceal hemorrhage. Prompt use of this lifesaving procedure is warranted.

Budd-Chiari syndrome revisited: 38 years' experience with surgical portal decompression.

OBJECTIVE: Ten years ago, we reported our results with what remains as the largest clinical experience with surgical portal decompression for Budd-Chiari syndrome (BCS) in the West. Since then, our series has expanded to 77 patients, and there has been an explosion of interest in and publications about BCS. The objectives of this study are to assess the validity of our observations and conclusions regarding BCS reported 10 years ago by expansion of our series of patients and observations of outcomes over an additional decade of close follow-up. METHODS: Seventy-seven patients with BCS were allocated to three groups: group I, 39 had hepatic vein occlusion alone, treated by side-to-side portacaval shunt (SSPCS); group II, 26 had inferior vena cava occlusion treated by mesoatrial shunt in eight and combined SSPCS and cavoatrial shunt (CAS) in 18; and group III, 12 had decompensated cirrhosis too late for portal decompression who were listed for liver transplantation (LT). An extensive diagnostic workup included angiography with pressure measurements and needle liver biopsy. Follow-up was 100%, lasting 5-38 years. RESULTS: In group I, long-term survival is 95% with 36 free of ascites, leading lives of good quality 5-38 years post-SSPCS. In group II, mesoatrial shunt was discontinued after 1990 because of a high failure rate, but combined SSPCS-CAS has resulted in 100% survival for 5-25 years. In group III, six patients (50%) are alive and well for more than 5 years post-LT. Serial liver biopsies following portal decompression have shown long-term reversal of the lesions of BCS. CONCLUSIONS: Long-term survival following portal decompression of BCS in the West has not been equaled by any other form of therapy, medical or surgical. It is imperative to perform surgical portal decompression early in the course of BCS in order to avoid irreversible liver damage.