New host record and molecular characterization of Dicauda atherinoidi Hoffman & Walker (Bivalvulida: Myxobolidae): a parasite of the emerald shiner Notropis atherinoides Rafinesque, 1818 and mimic shiner Notropis vollucellus Cope, 1865.

Updated morphological and histopathological descriptions for Dicauda atherinoidi (Bivalvulida:Myxobolidae) and an expanded host range are supplemented with the first molecular data and phylogenetic analyses of the genus. Plasmodia were located on the head, ventrum/body and fins of infected emerald shiner Notropis atherinoides Rafinesque, 1818 and mimic shiner Notropis vollucellus Cope, 1865, a new host species. Myxospores were spherical, ranging 9.3-11.4 µm (10.5 ± 0.4) in length, 9.0-11.0 µm (9.7 ± 0.4) in width and 6.6-7.0 µm (6.8 ± 0.2) thick in sutural view, and possessed 2-3 caudal processes (5.3-68.3 µm, 31.1 ± 13.6) connected to the spore body at the sutural groove, all of which are consistent with the genus Dicauda. In the absence of available Dicauda sequence data, the 18S rDNA sequences from Michigan isolates were most similar to Myxobolus spp. Phylogenetic analyses clustered these isolates with myxobolid species from cyprinid fish, suggesting these parasites may represent an underpopulated group of cyprinid-infecting myxozoans. Histopathology revealed thin-walled plasmodial pseudocysts in the dermis and associated connective tissue, where granulomatous inflammation and focal scale atrophy were also present. Further sampling/sequencing of myxobolids from Notropis spp. should expand these underrepresented myxozoans and offer further insight into Myxobolidae host family tropisms.

Accounting for disagreements on average cone loss rates in retinitis pigmentosa with a new kinetic model: Its relevance for clinical trials.

Since 1985, at least nine studies of the average rate of cone loss in retinitis pigmentosa (RP) populations have yielded conflicting average rate constant values (-k), differing by 90-160%. This is surprising, since, except for the first two investigations, the Harvard or Johns Hopkins' protocols used in these studies were identical with respect to: use of the same exponential decline model, calculation of average -k from individual patient k values, monitoring patients over similarly large time frames, and excluding data exhibiting floor and ceiling effects. A detailed analysis of Harvard's and Hopkins' protocols and data revealed two subtle differences: (i) Hopkins' use of half-life t0.5 (or t(1/e)) for expressing patient cone-loss rates rather than k as used by Harvard; (ii) Harvard obtaining substantially more +k from improving fields due to dormant-cone recovery effects and "small -k" values than Hopkins' ("small -k" is defined as less than -0.040 year(-1)), e.g., 16% +k, 31% small -k, vs. Hopkins' 3% and 6% respectively. Since t0.5=0.693/k, it follows that when k=0, or is very small, t0.5 (or t(1/e)) is respectively infinity or a very large number. This unfortunate mathematical property (which also prevents t0.5 (t(1/e)) histogram construction corresponding to -k to +k) caused Hopkins' to delete all "small -k" and all +k due to "strong leverage". Naturally this contributed to Hopkins' larger average -k. Difference (ii) led us to re-evaluate the Harvard/Hopkins' exponential unchanging -k model. In its place we propose a model of increasing biochemical stresses from dying rods on cones during RP progression: increasing oxidative stresses and trophic factor deficiencies (e.g., RdCVF), and RPE malfunction. Our kinetic analysis showed rod loss to follow exponential kinetics with unchanging -k due to constant genetic stresses, thereby providing a theoretical basis for Clarke et al.'s empirical observation of such kinetics with eleven animal models of RP. In contrast to this, we show that cone loss occurs in patients with increasing -k values during RP progression. And as the Hopkins' protocol selects more advanced RP cases than Harvard's to assure avoidance of ceiling effects (Harvard does this by kinetic monitoring), we show increasing -k kinetics to be the reason Harvard obtains more +k and small -k values. Thus the combined effects of (i) and (ii) produce Harvard's smaller average -k value. The relevance of the increasing biochemical stress model for optimizing clinical trials is discussed.

Rationale for an experimental treatment of retinitis pigmentosa: 140-month test of hypothesis with one patient.

BACKGROUND: Numerous mutations in over 100 rod genes are the well-established cause of apoptotic death of these cells and development of night blindness in retinitis pigmentosa (RP). Cone death is either concomitant or follows rod death with resultant loss of critical peripheral and central day vision. As cones are generally not encumbered by genetic mutations, the causes of their death and its prevention are the central problems of RP research. Currently no FDA-approved medications are available for retarding RP progression. HYPOTHESIS: It is proposed that cones, which are outnumbered 20:1 by rods, undergo apoptosis as a consequence of neurotrophic factor deficiencies and oxidative stresses accompanying massive rod death: increased retinal oxygen tension; leakage of lipid-peroxidation catalysts from disrupted membranes; reactive oxygen species from active/hyperactive microglia ingesting rod-apoptotic bodies. Accordingly we developed and tested a treatment regimen with a range of antioxidants in combination with the off-label use of deprenyl (1 mg/day), a safe antiapoptotic agent, which also upregulates eight neurotrophic factors. Since deprenyl inhibits only one of four mitochondrial apoptotic pathways, we added the antibiotic minocycline (100 mg/day) to our protocol at month 76. Minocycline complements deprenyl's therapeutic properties: it inhibits all four apoptotic pathways; inhibits apoptosis-initiating proteins; as phenol exerts powerful antioxidant properties; upregulates three antioxidant enzymes; downregulates oxidative/inflammatory microglia activities. Its safe long-term use for acne and rheumatoid arthritis received FDA approval; it passes the blood/brain and blood/retinal barriers readily; and because of its rapid and complete absorption causes no intestinal disturbances. The National Eye Institute has initiated in 2010 and 2011 clinical trials with minocycline (200 mg/day) for diabetic macular edema and retinal branch vein occlusion. TESTING OF HYPOTHESIS: The hypothesis was tested for 140 months with one RP patient monitored by Humphrey Perimetry, which was quantitated by two parameters: (a) sum of decibel units, (b) number of detected light sources (visual field). Although no decline was observed in these parameters during the first 50 months of treatment, they declined by 10-28% during months 50-65. These declines reversed upon introduction of minocycline: over the total 140-month treatment, the right eye visual field showed 0% decline and left eye 13.3% decline. Rate constants for logarithmic decline of visual field measured prior to treatment indicate that visual fields would have decreased by 64% and 70%, respectively by month 140 in the absence of treatment.

Statin use and neurologic morbidity after coronary artery bypass grafting: A cohort study.

BACKGROUND: Statin use before surgery has been associated with reduced morbidity and mortality after vascular surgery. The effect of preoperative statin use on stroke and encephalopathy after coronary artery bypass grafting (CABG) is unclear. METHODS: A post hoc analysis was undertaken of a prospectively collected cohort of isolated CABG patients over a 10-year period at a single institution. Primary outcomes were stroke and encephalopathy. Univariable analyses identified risk factors for statin use, which were applied to a propensity score model using logistic regression and patients were divided into quintiles of propensity for statin use. Controlling for propensity score quintile, the odds ratio (OR) of combined stroke and encephalopathy (primary endpoint), cardiovascular mortality, myocardial infarction, and length of stay were compared between statin users and nonusers. RESULTS: There were 5,121 CABG patients, of whom 2,788 (54%) were taking statin medications preoperatively. Stroke occurred in 166 (3.2%) and encephalopathy in 438 (8.6%), contributing to 604 patients (11.8%) who met the primary endpoint. The unadjusted OR of stroke/encephalopathy in statin users was 1.053 (95% confidence interval [CI] 0.888-1.248, p = 0.582). Adjustment based on propensity score resulted in balance of stroke risk factors among quintiles. The propensity score-adjusted OR of stroke/encephalopathy in statin users was 0.958 (95% CI 0.784-1.170, p = 0.674). There were no significant differences in cardiovascular mortality, myocardial infarction, or length of stay between statin users and otherwise similar nonusers. CONCLUSIONS: In this large data cohort study, preoperative statin use was not associated with a decreased incidence of stroke and encephalopathy after coronary artery bypass grafting.

Primary diagnosis and surveillance of white spot syndrome virus in wild and farmed crawfish (Procambarus clarkii, P. zonangulus) in Louisiana, USA.

This is the first report of natural white spot syndrome virus (WSSV) infection in wild and large-scale farmed crawfish. In the spring of 2007, 3 crawfish farms experienced heavy mortality in ponds populated by Procambarus clarkii and P. zonangulus. Histological examination revealed findings consistent with severe viral infection characterized by numerous intranuclear inclusions in ectodermal and mesodermal tissues. Samples tested by in situ hybridization, injection bioassay in Litopenaeus vannamei, and PCR (nested and real time) were all positive for WSSV. Samples were sent to the National Veterinary Services Laboratory in Ames, Iowa, USA, where WSSV was verified. Subsequently, a multi-parish survey of 184 sites in Louisiana (including farm and wild basin samples) using real-time PCR determined that >60% of sites sampled were positive for WSSV, including wild basin samples.

Is there cognitive decline 1 year after CABG? Comparison with surgical and nonsurgical controls.

BACKGROUND: It is widely assumed that decline in cognition after coronary artery bypass grafting (CABG) is related to use of the cardiopulmonary bypass pump. Because most studies have not included comparable control groups, it remains unclear whether postoperative cognitive changes are specific to cardiopulmonary bypass, general aspects of surgery, or vascular pathologies of the aging brain. METHODS: This nonrandomized study included four groups: CABG patients (n = 140); off-pump coronary surgery (n = 72); nonsurgical cardiac controls (NSCC) with diagnosed coronary artery disease but no surgery (n = 99); and heart healthy controls (HHC) with no cardiac risk factors (n = 69). Subjects were evaluated at baseline (preoperatively), 3 months, and 12 months. Eight cognitive domains and a global cognitive score, as well as depressive and subjective symptoms were analyzed. RESULTS: At baseline, patients with coronary artery disease (CABG, off-pump, and NSCC) had lower performance than the HHC group in several cognitive domains. By 3 months, all groups had improved. From 3 to 12 months, there were minimal intrasubject changes for all groups. No consistent differences between the CABG and off-pump patients were observed. CONCLUSIONS: Compared with heart healthy controls (HHC), the groups with coronary artery disease had lower cognitive test scores at baseline. There was no evidence that the cognitive test performance of coronary artery bypass grafting (CABG) patients differed from that of control groups with coronary artery disease over a 1-year period. This study emphasizes the need for appropriate control groups for interpreting longitudinal changes in cognitive performance after CABG.

Stroke after cardiac surgery: short- and long-term outcomes.

BACKGROUND: Stroke remains a devastating complication of cardiac surgery, but stroke prevention remains elusive. Evaluation of early and long-term clinical outcomes and brain-imaging findings may provide insight into stroke prognosis, etiology, and prevention. METHODS: Five thousand nine hundred seventy-one cardiac surgery patients were prospectively studied for clinical evidence of stroke. Stroke and nonstroke patients were compared by early outcomes. Data collected for stroke patients included brain imaging results, long-term functional status, and survival. Outcome predictors were then determined. RESULTS: Stroke was diagnosed in 214 (3.6%) patients. Brain imaging demonstrated acute infarction in 72%; embolic in 83%, and watershed in 24%. Survival for stroke patients was 67% at 1 year and 47% at 5 years. Independent predictors of survival were cerebral infarct type, creatinine elevation, cardiopulmonary bypass time, preoperative intensive care days, postoperative awakening time, and postoperative intensive care days. Long-term disability was moderate to severe in 69%. CONCLUSIONS: Stroke after cardiac surgery has profound repercussions that are independently related to infarct type and clinical factors. These data are essential for clinical decision making and prognosis determination.

The changing profile of the cardiac donor.

BACKGROUND: Expansion of traditional donor criteria has become standard in most centers. To determine how this has affected donor profiles, at our institution, we reviewed all adult (age > or = 16) cardiac donors of the past 15 years. METHODS: We separated 261 cardiac donors into 2 groups based on time periods: Group I, 1983 to 1991 (n = 131), and Group II, 1991 to 1998 (n = 130). RESULTS: The groups differed significantly in mean donor age (26.2 years vs 30.9; p < 0.001), percent older than 40 years (6% vs 27%; p < 0.001), percent female (23% vs 35%; p = 0.04), percent distant procurement (54% vs 22%; p < 0.001), and percent minority donors (14% vs 29%; p < 0.001). We found an increase in non-traumatic deaths (24% vs 40%; p = 0.008). Older donors had significantly more non-traumatic deaths than younger donors (79% vs 13%; p < 0.001). Overall 5-year survival of recipients was 64% and was not significantly different between our early and late experiences (60% vs 68%; p = not significant [NS]). Recipients with hearts from older donors had a 5-year survival similar to recipients with younger donor hearts (61% vs 64%; p = NS). Traumatic and non-traumatic donors had similar 5-year survivals (64% vs 63%, p = NS). A stepwise multivariate analysis of the entire cohort identified donor age, donor weight, recipient United Network for Organ Sharing status, and cardiopulmonary bypass time as significant independent risk factors for recipient survival. Recipients of hearts from donors < 90 kg had significantly better 5-year survivals than recipients from donors > or = 90 kg (66% vs 48%; p = 0.01). CONCLUSIONS: Our evolving cardiac donor pool now has more minorities, women, and older donors whose deaths are often non-traumatic. At our institution, donor pool expansion has had no adverse effect on the long-term survival of recipients.

Cerebral hemodynamics changes during retrograde brain perfusion in dogs.

The objective of this study was to examine cerebral hemodynamics changes during hypothermic circulatory arrest (HCA) with and without retrograde cerebral perfusion (RCP). Thirteen colony-bred hound dogs were placed on cardiopulmonary bypass (CPB) and cooled to 18 degrees C. Five dogs underwent 2 hours of HCA without RCP and 8 with RCP. The animals were then rewarmed on CPB until normothermic and weaned. Cerebral blood flow velocity (CBFV) and Gosling Pulsatility Index (PI) in the middle cerebral artery (MCA) were studied using trans-cranial Doppler ultrasound (TCD). At baseline and during pre- and postarrest CPB, there was anterograde direction of blood flow in the MCA. During HCA with RCP, there was retrograde direction of blood flow in the MCA. There was no difference in CBFV between pre-, during, and postarrest CPB in the group with RCP; however, there was significantly increased CBFV during postarrest CPB in the group without RCP compared to the dogs with RCP. Later, at 3 hours after postarrest CPB, there was decreased CBFV in all animals accompanied by increased PI (2.4 +/- 0.4 and 2.2 +/- 0.6 for animals with RCP and without RCP, respectively) and abnormal TCD waveform changes including decreased diastolic compartment and sharp systolic peak. During hypothermic circulatory arrest, RCP provides CBFV in the MCA comparable to MCA CBFV during CPB. HCA dogs without RCP showed immediate hyperemia on reperfusion. The decreased CBFV and increased PI at 1 hour after postarrest CPB could be an indicator of progressive ischemic injury due to the increased intracranial pressure despite the implementation of RCP.

Building a clinical program in a single institution.

A successful clinical program within either a single institution or a multi-institution complex requires the recruitment and retention of excellent faculty, a strong residency program, a successful, recognized research program, and leaders with administrative, organizational, and leadership skills.

Training women surgeons and their academic advancement.

The responsibility for those of us involved in residency training programs is to foster the development of future leaders in thoracic surgery. Although the actual training of female surgeons is no different than training male surgeons, academic advancement after training can be more difficult for women due to a variety of reasons. The education and training of female surgeons has its origin in admission to medical school followed by recruitment into a residency program. Following completion of a residency program, the retainment of women and men faculty should be the goal of departments and divisions of thoracic surgery. Specific recommendations are made for retainment of faculty. In addition to academic promotion and financial reward, creating the proper environment is an important consideration to allow women the chance to succeed in medicine. This report addresses the training aspects involved in the thoracic residency program and the state of professional academic advancement at the Johns Hopkins University School of Medicine.

Comparison of myocardial oxygen consumption using 11C acetate positron emission tomography scanning in a working and non-working heart transplant model.

OBJECTIVE: In acute cardiac rejection, changes in myocardial oxygen consumption occur; non-invasive detection of these metabolic changes would have obvious clinical utility. In the classic cervical, heterotopic, canine, transplant model, the heart is non-working. It has a low myocardial oxygen consumption. Creation of a working model with normal myocardial oxygen consumption would enhance validity of non-human studies. METHODS: Clearance of 11C acetate was determined by positron emission tomography (PET) scanning and compared with myocardial oxygen consumption in normal and transplanted canine hearts. Donor hearts from mongrel dogs (2.5-3 kg; n=4) were transplanted into the neck of adult beagles (12-15 kg; n=4), no immunosuppression was given. Two non-working hearts were modified to eject only coronary flow via the right ventricle. In two hearts, a novel working model was created with aortic regurgitation to load the left ventricle. Working and non-working hearts underwent PET scanning on post-operative days 2 and 4. Normal dog hearts (n=2) and native hearts of transplanted dogs (n=3) were used to validate the scanning technique. Coronary sinus and aortic oxygen saturation data along with myocardial blood flow (radiolabeled microspheres) confirmed that clearance of 11C acetate in normal and transplanted hearts followed a bi-exponential model. RESULTS: Myocardial oxygen consumption was correlated with the rate constant of 11C acetate rapid phase clearance (r=0.91) in normal and transplanted hearts. The working hearts had increased myocardial oxygen consumption compared to non-working hearts. CONCLUSIONS: This study (1) introduces a model of a working heterotopic cardiac transplantation with near-normal oxygen consumption; and (2) demonstrates that regional myocardial oxygen consumption in transplanted hearts can be detected by 11C acetate PET.

Pharmacologically induced preconditioning with diazoxide: a novel approach to brain protection.

BACKGROUND: Ischemic preconditioning is an endogenous mechanism whereby brief periods of ischemia render neurons resistant to subsequent lethal insults. This protection appears to alter cellular apoptosis and can be induced by potassium channel openers acting on the inner membrane of the mitochondria (mitoK(ATP)). To test the hypothesis that pharmacologic preconditioning could provide neuroprotection, the mitoK(ATP) opener diazoxide was used in a canine model of brain injury induced by hypothermic circulatory arrest (HCA). METHODS: Seventeen dogs were placed on cardiopulmonary bypass (CPB) and cooled to 18 degrees C. After 2 hours of HCA, animals were rewarmed and weaned from CPB. Six dogs received intravenous diazoxide (2.5 mg/kg bolus 15 minutes prior to CPB, then 0.5 mg/min until circulatory arrest, then restarted for the first hour of rewarming). Six animals received vehicle only. Five received diazoxide and the mitoK(ATP) blocker 5-hydroxydecanoate (5-HD). Using a modified Pittsburgh Canine Neurological Scoring System (0 = normal, 500 = brain death), animals were evaluated every 24 hours for 3 days. The brains were removed and histologic sections of four regions characteristically injured in this model were scored (0 = no injury, 4 = infarction) by a neuropathologist in a blinded fashion. RESULTS: Clinical scoring showed marked improvement in the diazoxide group at 48 hours (101 +/- 10.5 vs 165 +/- 14.8, p < 0.01) and 72 hours (54 +/- 9.3 vs 137 +/- 12.1, p < 0.01). This neuroprotection was attenuated when 5-HD was concomitantly administered. Three of four brain regions typically injured in this model (cortex, hippocampus, and entorhinal cortex) had significant neuron preservation in the diazoxide group. Likewise, combined region scores were significantly improved in the treatment group (1.18 +/- 0.2 vs 2.46 +/- 0.2, p < 0.01). CONCLUSIONS: Pretreatment with diazoxide resulted in significant improvement in both clinical neurologic scores and histopathology in our model of HCA. This suggests that pharmacologic preconditioning with the mitoK(ATP) channel opener diazoxide may offer effective neuroprotection during HCA.

The validity of self-reported drug use in non-treatment seeking individuals with cocaine dependence: correlation with biochemical assays.

Accurate estimate of drug exposure plays an important role in studies of the neurobiology of drug dependence. The validity of self-reported drug use by subjects participating in such studies has not been well established. This study examined the relationship between self-reported drug use and biological markers in 18 non-treatment-seeking cocaine-dependent individuals participating in research on the effects of cocaine on the brain. A significant relationship was found between self-reported frequency of cocaine use and hair cocaine concentration. Frequency of alcohol use correlated significantly with plasma carbohydrate-deficient transferrin and aspartate aminotransferase levels. These results suggest that self-reported substance use in non-treatment seeking research subjects is generally valid.

Selected contribution: measuring the response time of pulmonary capillary recruitment to sudden flow changes.

To determine how rapidly pulmonary capillaries recruit after sudden changes in blood flow, we used an isolated canine lung lobe perfused by two pumps running in parallel. When one pump was turned off, flow was rapidly halved; when it was turned on again, flow immediately doubled. We recorded pulmonary capillary recruitment in subpleural alveoli using videomicroscopy to measure how rapidly the capillaries reached a new steady state after these step changes in blood flow. When flow was doubled, capillary recruitment reached steady state in <4 s. When flow was halved, steady state was reached in approximately 8 s. We conclude that the pulmonary microcirculation responds rapidly to step changes in flow, even in the capillaries that are most distant from the hilum.

Etiology, pathogenesis, and experimental treatment of retinitis pigmentosa.

The paper provides an interdisciplinary evaluation of the etiology, pathogenesis, and experimental treatments of retinitis pigmentosa (RP). It addresses a 10-year controversy concerning the rate of progression of RP. One laboratory has estimated remaining visual field to be lost at a rate of 4.6% per year, whereas another laboratory estimates loss at 16-18%. This large discrepancy and lack of consensus needs resolution, since they pose serious statistical and operational problems for evaluating experimental treatment approaches to RP. The resolution of the controversy offered in the paper is based on a model of RP in which the initial rate of loss of visual field (the induction phase) is much slower than the subsequent logarithmic first-order rate of loss. The rationale for this kinetic model is that loss of mitochondrial function, possibly due to RP-genetically-related radical processes, has to reach a critical threshold value before the mitochondrial trigger of programmed cell death or apoptosis (i.e., the release of mitochondrial cytochrome c by the opening of the permeability transition pore, PTP) can be activated by an encounter with a second, but kinetically constant causative stress factor - most likely a light-stress-related factor. In its essential (two-causal) aspects, this kinetic model for RP is identical to the kinetic theories that have been proposed for the Gombertz human mortality plot. The described kinetic model for RP provides a solution to the visual field-loss controversy, since the first study was performed with a population containing a greater number of patients in the slow stage of RP than the second. Another objective of the investigation was to identify possible mechanisms of how the numerous genetic mutations in the rods of RP patients could give rise to damaging free-radical reactions capable of triggering apoptosis through their adverse effects on mitochondrial function. Another reason for focusing on radical reactions in RP was to provide a rationale for the proposed use of an extensive array of antioxidants and nutritional supplements for stemming progression of RP. In particular, the investigation focuses on saving cone-dependent central vision, i.e. on saving cells not affected by the genetic problems of the rods, but cells which can become lethally damaged by a spill-over of radicals and related harmful chemical reactions occurring in the rods.The third objective deals with the development of a rationale for a new strategy for retarding RP. This involves the use of desmethyldeprenyl, a metabolite of the anti-Parkinson's drug, deprenyl. The rationale is, in part, based on an observation that desmethyldeprenyl exerts antiapoptotic activities in a variety of neurodegenerative disorders. The protective mechanism involves the overexpression of the anti-apoptotic bcl-2 gene, leading to higher concentrations of bcl-2 proteins, which by binding to mitochondria inhibits the trigger mechanism of apoptosis - the opening of PTP and release of cytochrome C. At the same time, desmethyldeprenyl causes the underexpression of the pro-apoptotic bax gene, which via bax proteins facilitates the opening of the PTP. Both the anti-apoptotic and pro-apoptotic mechanisms appear to be mediated by the binding of desmethyldeprenyl to glyceraldehyde-3-phosphate dehydrogenase. Antiapoptotic effects can also be generated by the parent compound, deprenyl, when this is used daily in low concentrations of 1-2 mg/100 kg body weight. Under these conditions, it appears that the anti-apoptotic metabolite, desmethyldeprenyl, predominates over the pro-apoptotic metabolites of deprenyl, l -methamphetamine and l -amphetamine. Methamphetamine is not formed if desmethyldeprenyl is administered directly and thus could give desmethyldeprenyl a pharmacokinetic advantage over deprenyl. (ABSTRACT TRUNCATED)

Hypothermic circulatory arrest in octogenarians: risk of stroke and mortality.

BACKGROUND: The proportion of patients in their ninth decade of life undergoing complex cardiovascular procedures has increased over the past decade. The purpose of this study is to quantify the potential for stroke and mortality associated with deep hypothermic circulatory arrest (DHCA) in this age group. METHODS: At our institution, 251 adult patients had cardiovascular procedures that required DHCA since 1989. This included 20 patients 80 years of age or older (group I) and 231 patients less than 80 years (group II). Additionally, we analyzed 632 patients 80 years of age or older who underwent a variety of cardiovascular procedures since 1989 that required cardiopulmonary bypass but not DHCA (group III). Neurologic outcomes have been maintained in our database prospectively since 1991. RESULTS: The 30-day mortality in group I was 5%, in group II 15.2%, and in group III 8.2%. The stroke rate was 20% in group I, 8.8% in group II, and 6.5% in group III. CONCLUSIONS: DHCA can be performed with acceptable early mortality in patients in their ninth decade of life, but they are at an increased risk of stroke. Follow-up shows satisfactory late survival.