The AneuRx modular endograft device for the treatment of abdominal aortic aneurysms. Overview of 7 years of clinical use.

Open surgical repair of abdominal aortic aneurysms (AAAs) has been performed for over 40 years now with good results. However, the procedure continues to be high-risk with numerous potential complications. The AneuRx modular bifurcated endograft was one of the first to be tested to exclude AAAs via an endovascular approach. Data from multiple clinical trials show that treatment of AAAs with the AneuRx device is comparable to open repair with regards to mortality and may have improved short-term and long-term morbidities rates. The following review discusses clinical use of the AneuRx stent graft system from the initial clinical trial in 1996 to its current commercial use.

Intrathoracic herniation and perforation 18 years after open Nissen fundoplication.

Nissen fundoplication is the most commonly performed surgical procedure in the management of gastroesophageal reflux disease. Esophageal and gastric perforations most commonly occur in the perioperative period and carry significant morbidity. We describe a unique case of intrathoracic gastric wrap perforation and its suspected pathophysiology almost two decades after the original procedure.

Rabbit ventricular myocyte volume changes as a direct result of crystalloid cardioplegia in congestive heart failure induced by aortic regurgitation.

OBJECTIVES: We hypothesized that the cell volume of ventricular myocytes isolated from hearts in volume-overload congestive failure would respond differently to hypothermic cardioplegia than would sham-operated cohorts. METHODS: Adult rabbits underwent either valvotomy and aortic regurgitation-induced heart failure or sham surgery. Congestive failure was confirmed clinically and by means of echocardiography. Cell volumes of isolated myocytes were measured by digital video microscopy. After equilibration in 37 degrees C physiologic solution, cells were suprafused with 9 degrees C standard or low-Cl(-) St Thomas' Hospital solution followed by reperfusion in 37 degrees C physiologic solution. RESULTS: Exposure to cold St Thomas' Hospital solution for 20 minutes caused sham myocytes to swell by 8% (n = 9); cell volumes fully recovered on normothermic reperfusion. In contrast, congestive failure myocytes (n = 9) maintained their cell volume in cold St Thomas' Hospital solution and during reperfusion. Lowering the [K(+)][Cl(-)] product of St Thomas' Hospital solution by partially replacing Cl(-) with an impermeant anion prevented cellular edema in the sham group (n = 8) but caused a 4% swelling in failure myocytes (n = 10) on reperfusion. Osmotically shrinking the failure cells (n = 9) converted their behavior to that of sham cells. CONCLUSIONS: In the absence of ischemia, congestive failure myocytes are less sensitive to cardioplegia-induced edema than sham cells. Low-Cl(-) cardioplegia, which prevents edema and protects the normal heart, induced swelling and may be detrimental in myopathic hearts. Differences in volume regulation in failure and sham myocytes may be due to activation of volume-sensitive channels that are turned off by osmotic shrinkage.

Multiple left-sided cardiac lesions in one of Noonan's original patients.

We describe a complex case of obstruction of the left ventricular outflow tract in one of Dr. Noonan's original patients. Intraoperative findings revealed pathology at the valvar, subvalvar and supravalvar positions. Patients with Noonan syndrome are traditionally described as having right-sided cardiac pathology. Review of the literature revealed left-sided lesions to occur in a substantial number of these patients. We therefore suggest the routine employment of cardiac ultrasonography in all patients with Noonan syndrome with attention directed toward left-sided pathology, as well as the frequent pulmonary valvar pathology.

Age-related effects of St Thomas' Hospital cardioplegic solution on isolated cardiomyocyte cell volume.

OBJECTIVES: We tested the hypothesis that neonatal cells are more sensitive to cardioplegia-induced cell swelling than more mature cells and spontaneous swelling in the absence of ischemia can be prevented by cardioplegia with a physiologic KCl product. METHODS: Cell volumes of isolated ventricular myocytes from neonatal (3-5 days), intermediate (10-13 days), and adult (>6 weeks) rabbits were measured by digital video microscopy. After equilibration in 37 degrees C physiologic solution, cells were suprafused with 37 degrees C or 9 degrees C St Thomas' Hospital solution (standard or low Cl(-)) or 9 degrees C physiologic solution followed by reperfusion with 37 degrees C physiologic solution. RESULTS: Neonatal cells swelled 16.2% +/- 1.8% (P <.01) in 37 degrees C St Thomas' Hospital solution and recovered during reperfusion, whereas more mature cells maintained constant volume. In contrast, 9 degrees C St Thomas' Hospital solution caused significant age-dependent swelling (neonatal, 16.8% +/- 1.5%; intermediate, 8.6% +/- 2.1%; adult, 5.6% +/- 1.1%). In contrast to more mature cells, neonatal cells remained significantly edematous throughout reperfusion (8.1% +/- 1.5%). Swelling was not due to hypothermia because 9 degrees C physiologic solution did not affect volume. Lowering the KCl product of St Thomas' Hospital solution by partially replacing Cl(-) with an impermeant anion prevented cellular edema in all groups. CONCLUSION: In the absence of ischemia, neonatal cells were more sensitive to cardioplegia-induced cellular edema than more mature cells, and edema observed in all groups was avoided by decreasing the KCl product of St Thomas' Hospital solution to the physiologic range. Differences in cell volume regulation may explain the sensitivity of neonatal hearts to hyperkalemic cardioplegic arrest and suggest novel approaches to improving myocardial protection.