Quantitative investigation of cardiomyocyte hypertrophy and myocardial fibrosis over 6 years after cardiac transplantation.

OBJECTIVES: This study was performed to determine the degree and time course over 6 years of cardiomyocyte hypertrophy and myocardial fibrosis of the cardiac allograft in transplanted patients. BACKGROUND: Diastolic dysfunction and to a certain extent systolic dysfunction are common cardiac findings after heart transplantation. The development of posttransplant cardiomyocyte hypertrophy and myocardial fibrosis likely contributes to these derangements. METHODS: Cardiomyocyte diameter and percent fibrosis were determined in serial endomyocardial biopsy specimens obtained from 1 month up to 6 years following heart transplantation in 50 patients. Endomyocardial biopsy specimens from 40 patients with primary dilated cardiomyopathy and 11 normal subjects were similarly analyzed for control data. Analyses were performed in a blinded format using a validated computerized image analysis system (Optimas 5.2). RESULTS: Early (1 month) cardiomyocyte enlargement decreased to the smallest diameter 6 months posttransplant, but thereafter progressively increased by 10% to 20% over the subsequent 5- to 6-year period. Although not statistically established, principal stimuli may include a discrepancy in body size (recipient > donor), coronary allograft vasculopathy and posttransplant systemic hypertension. Percent myocardial fibrosis rose early (1 to 2 months) posttransplant and thereafter remained at the same modest level of severity. CONCLUSIONS: Cardiomyocyte diameter of the transplanted heart gradually increases over time, while percent myocardial fibrosis rises early and remains in a modestly elevated plateau after 2 months posttransplant. These histostructural changes likely contribute to the hemodynamic and cardiac functional alterations commonly observed posttransplant.

Effects of hypoproteinemia-induced myocardial edema on left ventricular function.

In previous studies, we observed left ventricular (LV) systolic and diastolic dysfunction in association with interstitial myocardial edema (IME) induced by either coronary venous hypertension (CVH) or lymphatic obstruction. In the present study, we examined the effects of myocardial edema induced by acute hypoproteinemia (HP) on LV systolic and diastolic function. We also combined the methods of HP and CVH (HP-CVH) to determine their combined effects on LV function and myocardial water content (MWC). We used a cell-saving device to lower plasma protein concentration in HP and HP-CVH groups. CVH was induced by inflating the balloon in the coronary sinus. Six control dogs were treated to sham HP. Conductance and micromanometer catheters were used to assess LV function. Contractility, as measured by preload recruitable stroke work, did not change in control or HP groups but declined significantly (14.5%) in the HP-CVH group. The time constant of isovolumic LV pressure decline (tau) increased significantly from baseline by 3 h in the HP (24.8%) and HP-CVH (27.1%) groups. The end-diastolic pressure-volume relationship (stiffness) also increased significantly from baseline by 3 h in the HP (78.6%) and HP-CVH (42.6%) groups. Total plasma protein concentration decreased from 5.2 +/- 0.2 g/dl at baseline to 2.5 +/- 0.0 g/dl by 3 h in the HP and HP-CVH groups. MWC of the HP (79.8 +/- 0.25%) and HP-CVH groups (79.8 +/- 0.2%) were significantly greater than that of the control group (77.8 +/- 0.3%) but not different from one another. In conclusion, hypoproteinemia-induced myocardial edema was associated with diastolic LV dysfunction but not systolic dysfunction. The edema caused by hypoproteinemia was more than twice that produced by our previous models, yet it was not associated with systolic dysfunction. CVH had a negative inotropic effect and no significant influence on MWC. IME may not have the inverse causal relationship with LV contractility that has been previously postulated but appears to have a direct causal association with diastolic stiffness as has been previously demonstrated.

Mechanical workload-myocardial water content relationship in isolated rat hearts.

We tested the hypothesis that the mechanical workload of the heart inversely determines the rate of myocardial edema formation in an isolated, perfused rat heart preparation. Heart rate (HR) was varied in three groups by pacing at 125 (HR125), 250 (HR250), or 350 beats/min (HR350). Left ventricular pressure (LVP) was varied in two additional groups by pacing at 250 beats/min and with the addition of either epinephrine (Epi) or propranolol (Pro) to the perfusate. In five otherwise identical groups, variation of coronary vascular resistance was minimized by adenosine. Myocardial water content (MWC) varied significantly and inversely with HR in the HR125, HR250, and HR350 groups. MWC of the HR250 group was significantly less than that of the Pro group but did not differ from the Epi group. However, when adenosine was used, MWC had significant inverse relationships with HR and LVP. We concluded that the mechanical workload of the heart inversely determines the rate and degree of myocardial edema formation in this isolated heart preparation, and both HR and LVP are determinants of this relationship.

Impairment of left ventricular function by acute cardiac lymphatic obstruction.

OBJECTIVES: We performed the following study to define the effects of acute cardiac lymphatic obstruction on left ventricular (LV) systolic and diastolic function. METHODS: Cardiac lymphatic obstruction was created in 8 pentobarbital-anesthetized dogs by identifying (Evans blue) and ligating the right and left epicardial lymphatics, the afferent and efferent lymphatics associated with the pretrachael and cardiac lymph nodes, and the thoracic duct. Left ventricular function was assessed by analysis of micromanometer-conductance catheter-derived LV pressure-volume relationships. Contractility was assessed by preload recruitable stroke work (PRSW). The active and passive phases of LV relaxation were assessed by the time constant o isovolumic relaxation (tau) and the end-diastolic pressure-volume relationship (stiffness), respectively. RESULTS: PRSW decreased significantly and tau increased significantly from baseline at 1, 2, and 3 h after cardiac lymphatic obstruction (n = 8), but stiffness did not change. Cardiac lymphatic obstruction had similar effects on LV function in a group of autonomically blocked dogs (n = 5). Left ventricular function did not change in sham treated controls (n = 8). Cardiac lymphatic obstruction induced a significant increase in LV wet/dry weight ratios (3.58 +/- 0.01) when compared to the control group (3.53 +/- 0.02). Histopathology of the myocardium in the lymphatic obstruction groups revealed significant lymphangiectasis and increased interstitial spacing when compared to controls. CONCLUSIONS: Acute cardiac lymphatic obstruction depresses contractility and active relaxation and causes mild LV myocardial edema, but does not alter diastolic stiffness.

Posttransplantation lymphoproliferative disorder in cardiac transplant allografts.

Posttransplantation lymphoproliferative disorder occurs in 1.5% to 13% of heart transplant recipients and rarely involves the allograft. We report a case of posttransplantation lymphoproliferative disorder restricted to the mitral valve in a heart transplant recipient. Thirteen cases of cardiac allograft involvement by posttransplantation lymphoproliferative disorder are reported in the literature. None are restricted to the allograft. Five specify sites of cardiac involvement. Valvular masses without infection necessitate evaluation for posttransplantation lymphoproliferative disorder involvement of the cardiac allograft valve.

A comparison of isoflurane versus fentanyl as primary anesthetics for mitral valve surgery.

We conducted a randomize study of fentanyl compared to isoflurane anesthesia in patients with pulmonary hypertension undergoing mitral valve surgery. Patients were premedicated and randomly assigned to one of two groups: 21 patients had anesthesia induced with thiopental and maintained with isoflurane; 23 patients had anesthesia induced with a fentanyl bolus and maintained with a fentanyl infusion. Adjustments of fentanyl infusion and isoflurane concentration, as well as fentanyl boluses and vasoactive/positive inotropic medication, were administered to maintain preoperative arterial blood pressure. Both groups exhibited similar demographics, similar duration of cardiopulmonary bypass (CPB) surgery, anesthesia, and time from entrance into the surgical intensive care unit (SICU) to endotracheal extubation. However, the time from entrance into the SICU to awake was significantly (P < 0.05) shorter in patients given isoflurane anesthesia. Hemodynamic variables were recorded at baseline and 12 surgical events and compared between and within groups. Significant changes from baseline were demonstrated in both groups upon institution and discontinuation of CPB. Patients receiving isoflurane anesthesia exhibited cardiovascular depression as compared to their baseline. There were no deaths in either patient group. Adequate hemodynamic profiles were achieved in both groups with comparable use of inotropic and vasoactive medication, with the exception of norepinephrine that was administered intraoperatively to significantly (P < 0.05) more patients in the isoflurane-based anesthesia group. Neither technique was associated with acute improvement of right heart performance or pulmonary hypertension, in large part because of morphologic changes of the pulmonary arterial bed, occurring with long-standing mitral valve disease. We conclude that isoflurane-based anesthesia is adequate for this type of surgery, although there is a higher anesthetic algorithm failure rate than with fentanyl-based anesthetic technique.

Acute transient coronary sinus hypertension impairs left ventricular function and induces myocardial edema.

This study was performed to evaluate the direct and indirect effects of acute coronary sinus hypertension (CSH) on systolic and diastolic left ventricular (LV) function. Coronary sinus pressure was elevated to 25 mmHg for 3 h in eight pentobarbital-anesthetized dogs and then relieved. LV contractility was assessed by preload recruitable stroke work (PRSW) and end-systolic elastance (Ees). Diastolic function was assessed by the time constant of isovolumic relaxation (tau) and the end-diastolic pressure volume relationship (EDPVR). PRSW and Ees decreased progressively, and tau and the slope of the EDPVR increased progressively with CSH. These changes persisted after relief of CSH. beta-Adrenergic and cholinergic receptor blockade, performed in six dogs, did not alter the effects of CSH on systolic or diastolic function. The LV wet-to-dry weight ratios of the groups with CSH were significantly greater than those of a control group without CSH. We conclude that CSH results in changes in the left ventricle that depress contractility, prolong active relaxation, and increase diastolic stiffness. The dysfunction was not the direct effect of CSH or autonomic reflex activation, but may have been induced by fluid accumulation within the interstitium.

Effects of acid aspiration-induced lung injury on left ventricular function.

BACKGROUND: Acid aspiration-induced acute lung injury (AALI) leads to myocardial leukosequestration and edema in rats and hemodynamic depression in dogs, but the effects of AALI on left ventricular (LV) function have not been carefully studied. METHODS: We examined the effects of 0.1 N HCl administration into the lung on LV function, leukosequestration, and edema in pentobarbital-anesthetized, atropinized (n = 8), or autonomically blocked (n = 7) dogs. Saline solution was administered into the lungs of a control group of autonomically blocked dogs (n = 6). LV contractility was assessed by end-systolic elastance (EES) and preload recruitable stroke work (PRSW). Active relaxation was assessed by the time constant of LV pressure decline (tau). RESULTS: AALI resulted in significant (p < 0.05) decreases in mean arterial pressure and cardiac output and increases in pulmonary artery pressure and systemic vascular resistance in atropinized and autonomically blocked dogs but not in saline control group. In atropinized dogs tau did not change after injury, but EES and PRSW were increased significantly at 2 and 3 hours after injury, despite significant myeloperoxidase activity and extravascular fluid wet-dry weight ratios. EES, PRSW, and tau did not change in the autonomically blocked dogs in response to AALI or in the saline control group. CONCLUSIONS: We concluded that AALI results in a baroreflex mediated enhancement of LV contractility in dogs, despite mild myocardial leukosequestration and edema formation.

Neuropsychological function in patients with end-stage heart failure before and after cardiac transplantation.

This study was performed to examine cognitive function in patients with end-stage heart failure, to identify possible cardiovascular factors associated with cognitive function, and to evaluate changes in cognitive function in a subgroup of patients who received heart transplantation. An extensive battery of neuropsychological tests were given to 62 patients with end-stage cardiac failure as part of their evaluation for cardiac transplantation. Most patients were consecutive referrals, not selected because of cognitive complaints. A small subgroup of transplanted (n = 7) and non-transplanted (n = 4) patients received a repeat neuropsychological examination. At initial examination, approximately 50% of the patients met criteria for impairment in reference to normal control values. Higher stroke volume index and cardiac index and lower right atrial pressure were correlated with better cognitive function. In the subgroup of patients re-examined, the transplanted patients demonstrated significantly improved cognitive function, whereas the non-transplanted subjects were unchanged. These data indicate that in patients with end-stage heart failure there is a high prevalence of impaired cognitive function which is related to measures of cardiovascular efficiency. Preliminary evidence suggests that these impairments may be partially ameliorated by cardiac transplantation.

Left atrial volumes and function in orthotopic cardiac transplantation.

Early ventricular filling and therefore passive left atrial emptying may be impaired in patients with cardiac transplantation. As a result, left atrial function may be an important factor in maintaining stroke volume in recipients of orthotopic cardiac transplants. Left atrial volumes maximal (mitral valve opening), minimal (mitral valve closure), and onset of atrial systole (P wave on electrocardiogram) were determined by echocardiography using the biplane area-length method in 12 patients after cardiac transplantation and 12 control subjects. Maximal and minimal left atrial volumes and left atrial volumes at onset of atrial systole were larger in patients who had cardiac transplantation than in control subjects (89.8 vs 41.8 cm3, 48 vs 15.2 cm3, and 70.4 vs 27.0 cm3, respectively; p < 0.01). In patients undergoing cardiac transplantation, good correlations were found between left atrial maximal volume and left ventricular mass (r = 0.56) and between left atrial maximal volume and mean pulmonary capillary wedge pressure (r = 0.81). Left atrial passive emptying volume (maximal minus volume at P wave), was not statistically different between the two groups (19.3 in patients receiving transplants vs 14.7 cm3 in control subjects), but left atrial stroke volume (beginning atrial systole to minimal) was larger in patients receiving transplants than in control subjects (22.4 vs 11.8 cm3, respectively; p < 0.001). Thus left atrial contraction contributed 42% to the left ventricular stroke volume in patients who had cardiac transplantation but only 17% in control subjects (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute lung injury isolated to an in situ lung preparation causes sustained reflex cardiovascular depression in dogs.

We tested the hypothesis that acute lung injury (ALI) isolated to a perfused in situ left lung preparation results in sustained reflex cardiovascular depression. Phorbol myristate acetate (PMA), an agent that activates neutrophils, administered into the isolated lung preparation of chloralose-anesthetized dogs resulted in ALI, as assessed by wet-to-dry weight ratios and histopathology, and significant decreases in heart rate (43%), mean arterial pressure (27%), aortic blood flow (29%) and maximum rate of change in left ventricular pressure (30%). Significant reflex effects occurred by 20 min after PMA administration and were sustained for 40 min (n = 7). Hemodynamic variables recovered when the left lung was denervated 60 min after PMA administration. Indomethacin administered into the isolated circulation before PMA (n = 5) did not significantly influence the ALI or reflex effects. Systemic atropinization (n = 6) prevented only the bradycardia. Left lung denervation before ALI (n = 3) prevented all reflex effects. We conclude that PMA administration into an isolated in situ lung preparation results in ALI and sustained reflex cardiovascular depression that is most likely elicited by pulmonary C-fiber stimulation and mediated by withdrawal of sympathetic efferent nerve activity.

Vagal innervation influences the whole body oxygen consumption-delivery relationship in the dog.

Vagotomy alters regional blood flow distribution by interrupting the tonic central inhibitory effect of cardiopulmonary vagal afferent nerves on sympathetic outflow predominantly to the renal, splanchnic, and cutaneous circulations. We hypothesized that the alteration of blood flow distribution by vagotomy would lead to disruption of the oxygen consumption-oxygen delivery relationship (VO2/DO2), increase critical DO2 (DO2Crit), and decrease whole-body oxygen extraction ratio (O2ER). Nineteen chloralose-anesthetized, paralyzed, splenectomized dogs were submitted to either bilateral vagosympathectomy (n = 7), bilateral vagotomy (n = 6), or sham denervation (n = 6) following baseline cardiorespiratory parameter measurement. VO2 was measured by indirect calorimetry and carotid blood flow by ultrasonic flow probe. Incremental hemorrhages (1-5 mL/kg) were performed to determine the VO2/DO2 relationship. Cardiorespiratory parameters were measured after each hemorrhage at steady-state VO2. DO2Crit was derived from the VO2/DO2 relationship using a best-fit regression analysis technique. The average DO2Crit values of the vagotomy (9.1 +/- .54) and vagosympathectomy (11.5 +/- 1.2 mL/min/kg) groups were significantly greater than the control group (7.72 +/- .43). After hemorrhage had been performed to a point that decreased mean arterial pressure to approximately 70 mmHg from baseline values, carotid blood flow in the vagosympathectomy group was significantly greater than the control group. We conclude that vagotomy disrupts the VO2/DO2 relationship. Vagosympathectomy causes a severe disruption of the VO2/DO2 relationship, probably by the combined effect of vagotomy and interruption of sympathetic nervous system control of blood flow to the head and neck.

Timing of recipient atrial contraction: a major determinant of transmitral diastolic flow in orthotopic cardiac transplantation.

The effect of recipient left atrial contraction on diastolic transmitral flow was studied in eight asymptomatic heart transplant patients (seven men and one woman, mean age 51.8 +/- 9.7 years) with normal left ventricular systolic function. The transmitral flow velocity profile was evaluated in 326 beats (mean 40.8 +/- 12 beats, range 20 to 58 beats/patient). Recipient left atrial contraction was classified as early diastolic, late diastolic, and systolic. Results showed: (1) early diastolic transmitral flow velocity integral (in centimeters) was lower (p < 0.05) following late diastolic recipient left atrial contractions (7.5 +/- 2.1) compared with early diastolic (10.1 +/- 2.7) or systolic (8.5 +/- 1.5) recipient left atrial contractions; (2) late diastolic transmitral flow velocity integral was higher following late diastolic (4.7 +/- 1.8) compared with systolic (4.1 +/- 1.9) recipient left atrial contractions and was virtually abolished (0.45 +/- 14) following early diastolic recipient left atrial contractions; and (3) total diastolic transmitral flow velocity integral was significantly higher (p < 0.05) following late diastolic and systolic (12.2 +/- 2.8 and 12.0 +/- 2.5) compared with early diastolic left atrial contractions (10.5 +/- 2.8). Thus recipient left atrial contraction is a significant determinant of the transmitral diastolic flow pattern in heart transplant patients. Variations in the timing of recipient left atrial contraction may lead to fluctuations of diastolic flow and may compromise cardiac output.

Catheter-induced pulmonary artery rupture in the setting of cardiopulmonary bypass.

Pulmonary artery rupture is an infrequent complication of flow-directed catheters. Because cardiopulmonary bypass offers an opportunity for control of gas exchange and hemorrhage, pulmonary artery rupture in this setting is different from that occurring in the intensive care unit and catheterization laboratory. A collective review of 30 published cases was conducted. Sixty-nine percent of patients were female and 50% had valvular heart disease. The right pulmonary artery was injured in 93% of cases. Arterial rupture presented with airway hemorrhage in 29 of 30 patients. Six patients presented with a herald airway bleed after catheter insertion but before operation. Three of 4 patients died when operation was performed in the face of a herald bleed. Airway hemorrhage most commonly developed during bypass weaning (19 cases). Recurrent hemorrhage occurred in 45% of patients (9/20) treated conservatively compared with 0% (0/7) in those having surgical control of bleeding (p = 0.07). Three patients died in the operating room. Overall mortality was 41%. Uncontrolled hemorrhage was the leading cause of death. Conservative management strategies are associated with a high incidence of secondary, often fatal, hemorrhage. Although pulmonary resection controls bleeding, mortality from other causes is a problem. A treatment protocol is proposed that considers these management dilemmas.

Intraoperative and postoperative effects of vancomycin administration in cardiac surgery patients: a prospective, double-blind, randomized trial.

OBJECTIVES: In response to an increased frequency of Staphylococcus epidermidis infections in postoperative cardiac surgery patients, antibiotic prophylaxis was changed to include both vancomycin and cefazolin pre- and intraoperatively. Subsequent to the addition of vancomycin prophylaxis, clinical impression and retrospective analysis supported a correlation between vancomycin administration and post-cardiopulmonary bypass norepinephrine use. DESIGN: A prospective, double-blind, randomized study. SETTING: Tertiary care center in a university hospital. PATIENTS: A total of 58 patients undergoing elective coronary artery bypass surgery under high-dose fentanyl anesthesia. INTERVENTIONS: Patients were randomized to receive cefazolin and either vancomycin or normal saline pre-, intra-, and postoperatively in a double-blinded protocol. MEASUREMENTS AND MAIN RESULTS: Hemodynamic profiles and doses of administered vasoactive agents were calculated and recorded for all patients for both intra- and postoperative time periods. Hypotension consistent with vasodilation was treated with a norepinephrine infusion. The rate and frequency of norepinephrine infusions were tabulated for both groups. Hemodynamic profiles that were obtained after the administration of the initial dose of vancomycin or normal saline and before the induction of general anesthesia and those profiles obtained after the induction of general anesthesia until the initiation of cardiopulmonary bypass showed no difference between groups and no evidence of vasodilation secondary to vancomycin administration. However, subsequent doses of vancomycin in the intra- and postoperative periods were associated with a significantly greater frequency of norepinephrine infusions to maintain normal hemodynamic indices. In the vancomycin group, 50% of patients received a norepinephrine infusion in the intra- and/or postoperative period as compared with 14% in the normal saline group (p < .01). Furthermore, the group of patients who received vancomycin and subsequently required a norepinephrine infusion had significantly lower mean systolic arterial pressure, mean arterial pressure, and systemic vascular resistance as compared with all other groups. There were no differences between groups in the use of vasopressors (other than norepinephrine) or fluid balance. CONCLUSIONS: The results show that a significantly greater number of patients who received vancomycin required a norepinephrine infusion and that, despite norepinephrine infusion therapy, systemic vascular resistance was not normalized in this group of patients. The study supports the conclusion that perioperative administration of vancomycin in cardiac surgery patients may result in hypotension requiring the use of a vasopressor in an attempt to normalize hemodynamic indices.

The significance and prevention of air emboli with the total artificial heart.

Embolism remains a significant complication of the total artificial heart (TAH). The ineffectual deairing of the TAH can allow embolization of the retained air. The standard needle aspiration of TAH air (Group A) was compared with a new protocol (Group B) that included standard needle TAH aspiration plus simultaneous pumping of the TAH against an occluded ascending aorta and main pulmonary artery with vacuum applied to a needle in the proximal aorta and pulmonary artery. There were 4 calves in each group. There was no premortem evidence of systemic or pulmonary emboli. Both groups of animals were electively terminated less than 2 weeks postoperatively Postoperative mean aortic and pulmonary artery pressures were recorded for each animal. Animals in Group B had a significant decline in pulmonary artery pressures (43 +/- 12 vs. 33 +/- 8 mm Hg) 1 h after TAH implantation when compared with Group A. All other aortic and pulmonary artery pressure differences between Groups A and B were not statistically significant within 24 h of the operation. Group A animals had a 75% incidence, and Group B animals had 100% incidence of TAH thrombus. This very small thrombus was found exclusively at the inflow valve-TAH housing interface. Evaluation of the kidneys postmortem was used to identify embolic injury. All animals in Group A had evidence of acute, hemorrhagic injury, but none of the Group B animals had similar injury. Half of the animals in each group had small, fibrotic chronic renal cortical injury, which did not develop during TAH implantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of successful cardiac transplantation on plasma endothelin.

After cardiac transplantation, cyclosporine-treated patients exhibit a high incidence of systemic hypertension, the mechanism of which is not known. Endothelin, a potent vasoconstrictor peptide of endothelial origin, may be activated by cyclosporine-induced endothelial injury and therefore may mediate post-transplant hypertension. In the present study, we tested whether immunoreactive endothelin-1 could be detected by radioimmunoassay in the plasma of cardiac transplant recipients and if levels correlated with hemodynamic characteristics, cyclosporine level, or renal function as assessed by serum creatinine. Plasma endothelin was measured in 22 stable cyclosporine-treated patients 9 days to 3 years after successful orthotopic cardiac transplantation before routine hemodynamic assessment and surveillance endomyocardial biopsy. Fifteen patients were receiving chronic therapy for hypertension. Plasma endothelin-1 was 5.2 +/- 1.8 pg/ml (range 3.1 to 10.5), which was increased compared with that in 12 normal subjects (1.9 +/- 0.3 pg/ml; range 1.4 to 2.4); the difference was statistically significant (p < 0.0001). Repeated sampling in 8 patients at weekly intervals identified a persistent increase in endothelin with only modest variability. Endothelin-1 did not correlate with any hemodynamic variable, serum creatinine or cyclosporine level. Thus, endothelin-1 is increased after successful orthotopic cardiac transplantation. In the absence of discrete correlations with hemodynamic variables, serum creatinine or cyclosporine levels, both the characteristics and mechanisms for increased endothelin in recipients of cardiac transplants require further evaluation.

A limited axillary thoracotomy as primary treatment for recurrent spontaneous pneumothorax.

Recurrent spontaneous pneumothorax often requires surgical treatment following variable periods of chest tube therapy. A limited axillary thoracotomy provides sufficient exposure to isolate or excise pulmonary blebs and perform a pleurodesis. Prompt use of this surgical approach in lieu of the initial placement of a thoracostomy tube avoids prolonged hospitalization and a significant failure rate of thoracostomy tubes to resolve this problem. This operation can also prevent recurrence, a significant problem for this pathologic process. Fourteen patients with recurrent spontaneous pneumothorax underwent an axillary thoracotomy as either primary treatment or within 72 h of thoracostomy tube placement. The average follow-up was 38 months for the initial 10 patients and 23 months for the entire group. The procedure averaged 66 min in duration. The average incision was 3.3 cm in length. There was an equal male/female ratio and right-left distribution. The patients were discharged an average of 4.2 days after surgery. There were no complications. The most recent six patients with a recurrent pneumothorax were surgically treated on the day of admission without a preoperative chest tube. The other eight patients had a thoracostomy tube for control of the pneumothorax, with surgery performed within 72 h of tube placement. A limited axillary thoracotomy corrected the underlying pathology, hastened hospital discharge, limited pain, prevented short-term recurrence, and was cosmetically acceptable. A limited axillary thoracotomy is the operation of choice when a spontaneous pneumothorax requires surgery. This surgical approach has become our primary treatment for recurrent pneumothorax, avoiding the use of a preoperative thoracostomy tube and unnecessary delay, with excellent results for the patient.

Comparative study of cefazolin, cefamandole, and vancomycin for surgical prophylaxis in cardiac and vascular operations. A double-blind randomized trial.

Three-hundred twenty-one adults undergoing cardiac or major vascular operations were randomized to receive intravenous cefazolin, cefamandole, or vancomycin for prophylaxis against surgical infection in a double-blind trial. All three regimens provided therapeutic blood levels throughout operation in patients studied undergoing cardiopulmonary bypass. The prevalence of surgical wound infection was lowest with vancomycin (4 infections [3.7%] versus 14 [12.3%] and 13 [11.5%] in the cefazolin and cefamandole groups, respectively; p = 0.05); there were no thoracic wound infections in cardiac operations in the vancomycin group (p = 0.04). The mean duration of postoperative hospitalization was lowest in the vancomycin group (10.1 days; p < 0.01) and highest in the cefazolin group (12.9 days). Prophylaxis with vancomycin or cefamandole, compared with cefazolin, did not prevent nosocomial cutaneous colonization by methicillin-resistant coagulase-negative staphylococci; colonization or infection with vancomycin-resistant staphylococci or enterococci was not detected. Adverse effects attributable to the prophylactic regimen were infrequent in all three groups. Eight patients given vancomycin became hypotensive during administration of a dose, despite infusion during a 1-hour period; however, slowing the rate of administration and pretreating with diphenhydramine allowed vancomycin to be resumed and prophylaxis completed uneventfully in five of the patients. We conclude that administration of vancomycin (approximately 15 mg/kg), immediately preoperatively, provides therapeutic blood levels for surgical prophylaxis throughout most cardiac and vascular operations, resulting in protection against postoperative infection superior to that obtained with cefazolin or cefamandole. Vancomycin deserves consideration for inclusion in the prophylactic regimen (1) for prosthetic valve replacement and prosthetic vascular graft implantation, to reduce the risk of implant infection by methicillin-resistant coagulase-negative staphylococci and enterococci; (2) for any cardiovascular operation if the patient has recently received broad-spectrum antimicrobial therapy; and (3) for all cardiovascular operations in centers with a high prevalence of surgical infection with methicillin-resistant staphylococci or enterococci. Guidelines for dosing and administration of vancomycin for cardiovascular surgical prophylaxis are provided.