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Biomedical subjects

M J Curtis

Publications and source records attributed to M J Curtis.

At least 19 recordsLinked to original sources
PubMed1992

Musculoskeletal injuries in the Afghan war.

Among the 1274 patients admitted to a Pakistan border hospital from 1985 to 1987, the distribution and outcome of musculoskeletal war injuries differed from those seen in other conflicts. Serious complications from injuries were found in approximately 50 per cent of patients, of which most were wound infections, chronic osteomyelitis, and restriction of joint motion. Guerrillas in the Afghan war had no access to acute medical treatment in the field. Many patients died before reaching the hospital, as reflected in the low proportion of paraxial injuries; very high complication rates were noted for all injuries. Although some complications, such as soft tissue infection and foreign body retention are not site specific, other complications such as contracture, non-union, loss of range of motion, and chronic osteomyelitis are highly related to the region injured. Early surgical management and evacuation of those with musculoskeletal war injuries can greatly improve the outcome from war trauma and reduce the subsequent disability. However, the increasing use of hand-held anti-aircraft missiles may prevent the rapid evacuation of the wounded in future conflicts, and may make the situation seen in Afghanistan more common.

Adolescent↗
PubMed1992

Computerized templating in uncemented total hip arthroplasty to assess component fit and fill.

The aim of the uncemented femoral component in total hip arthroplasty is to achieve a stable bone-prosthesis interface without the use of polymethyl methacrylate (PMMA). Maximal fill of the femoral canal by the prosthesis promotes initial stability and long-term optimal stress transfer to the bone. The percentage "fit and fill" of the proximal femur by three prostheses, the porous coated anatomic, anatomic medullary locking, and the Harris-Galante, was compared by use of a computerized templating model to assess preoperative radiographs of 20 patients. Results showed that overall percentage fit and fill was similar and satisfactory (greater than 60%) in 17 of 20 patients. If a satisfactory fill was not achieved with one prosthesis, another prosthesis did not significantly improve fill. Lack of bony contact in the proximomedial femur was the most common deficiency noted.

Computer-Aided Design↗
PubMed1992

A modified model of global ischaemia: application to the study of syncytial mechanisms of arrhythmogenesis.

OBJECTIVE: The aim was to develop a simple modified global ischaemia preparation to study the relation between ischaemic zone size and the incidence of ischaemia induced and reperfusion induced arrhythmias, to test the hypothesis that arrhythmias are initiated by flow of injury current between the ischaemic zone and the uninvolved myocardium. The new model was used to examine whether injury current suppression is involved in the mechanism of action of a new antiarrhythmic intervention, substitution of chloride anion by nitrate. METHODS: Isolated perfused (Langendorff mode) rat hearts (n = 12 per group) were subjected to 30 min global or regional ischaemia. Ventricular arrhythmia incidence during ischaemia and during reperfusion were related to the size of the involved region. The modified model of global ischaemia employed right intra-atrial superfusion to maintain normal sinus rate and 1:1 atrioventricular (AV) conduction. RESULTS: Sham ligation, low left coronary ligation, high left coronary ligation, and global ischaemia produced, as a percentage of total ventricular weight, 0%, 21.0(SEM 0.8)%, 47.0(1.0)%, and 100% regions of ischaemia (occluded zones). Heart rates were similar in each group and AV block did not occur. The incidences of ischaemia induced ventricular fibrillation (VF) were 0, 17, 75, and 17% with increasing occluded zone sizes. Incidences of reperfusion induced VF were 0, 8, 92, and 92% respectively. The antiarrhythmic action of substitution of extracellular chloride by nitrate, previously shown using models of regional ischaemia, was confirmed in the modified global ischaemia model. CONCLUSIONS: These findings strongly support the theory that current of injury between ischaemia and adjacent non-ischaemic zones is necessary for initiation of ischaemia induced VF, since susceptibility was maximal when ischaemic and uninvolved regions were equivalent in size (and the scope for injury current was maximal) whereas susceptibility was negligible when scope was minimal. In contrast, reperfusion induced VF appears to depend only on the presence and amount of reperfused tissue, indicating that flow of injury current between involved and uninvolved tissue is unnecessary for its initiation. Discrimination of the mechanism of action of antiarrhythmic interventions may be possible since drugs effective solely via amelioration of flow of injury current (or incrementation of collateral flow) will not influence arrhythmias in this model. Modification of injury current and collateral flow do not appear to contribute to the antiarrhythmic action of substitution of extracellular chloride by nitrate.

Animals↗
PubMed1992

Anion manipulation: a new antiarrhythmic approach. Action of substitution of chloride with nitrate on ischemia- and reperfusion-induced ventricular fibrillation and contractile function.

The role of anions in the initiation of ischemia- and reperfusion-induced arrhythmias is unknown. We examined the antiarrhythmic effects of isotonic substitution of extracellular Cl- with NO3- by using the rat Langendorff preparation (n = 12 per group). During 30 minutes of regional ischemia, the incidence of ventricular fibrillation (VF) was reduced from 50% in hearts perfused with control solution (containing a Cl-:NO3- ratio of 100:0) to 25%, 0% (p less than 0.05), 0% (p less than 0.05), and 0% (p less than 0.05) by perfusion with solution containing Cl-:NO3- ratios of 75:25, 50:50, 25:75, and 0:100, respectively. The incidence of reperfusion-induced VF was also reduced from 58% to 25%, 8% (p less than 0.05), 8% (p less than 0.05), and 0% (p less than 0.05), respectively. Similar effects were produced in hearts reperfused after briefer durations of ischemia (10 or 15 minutes). Substitution of NO3- for Cl- also facilitated spontaneous termination of VF. Heart rate and occluded zone size were not affected by anion manipulation. Coronary flow was affected by NO3-, but changes did not correlate with arrhythmias. During ischemia, electrocardiographic changes indicative of class III activity (widening of the ventricular complex) were produced by anion substitution. These changes occurred selectively in the ischemic tissue with no significant influence before ischemia onset. However, the relation between this effect and arrhythmia reduction was not linear and a cause-effect relation is therefore unlikely. In separate groups of hearts (n = 12 per group), switching from 100:0 to 0:100 Cl-:NO3- solution or vice versa 10 seconds after coronary occlusion or just before reperfusion demonstrated that 1) protection against ischemia-induced VF resulted partly from an action in the ischemic zone and partly from an action in the nonischemic zone, and 2) protection against reperfusion-induced VF resulted principally from an action occurring during reperfusion and within the reperfused tissue. To assess whether benefit was offset by deleterious effects on contractile function in nonischemic tissue, we constructed Starling curves in isolated rate hearts. The 0:100 Cl-:NO3- solution had no effect on compliance or contractility at physiological end-diastolic pressures but reduced the slope of the peak systolic pressure-volume relation by approximately 20% as end-diastolic pressure was increased above 10 mm Hg. In conclusion, anions appear to play a hitherto unrecognized role in arrhythmogenesis in ischemia and reperfusion. Manipulation of anion homeostasis may represent a novel target for antiarrhythmic drug development.

Animals↗
PubMed1992

The initial stability of uncemented acetabular components.

The osseo-integration of an uncemented acetabular component depends on its initial stability. This is usually provided by under-reaming of the acetabulum. We have assessed the fixation of 52 mm porous-coated hemispherical prostheses inserted into cadaveric acetabula under-reamed by 1, 2, 3 and 4 mm. We tested the torsional stability of fixation, after preloading with 686 N in compression, by measuring the torque required to produce 1 degree and 2 degrees of rotation. Under-reaming by 2 mm and 3 mm gave significantly better fixation than 1 mm (p less than 0.01, p less than 0.02). Insertion after under-reaming of 4 mm caused some fractures. To obtain maximum interference fit and optimal implant stability, we recommend the use of an implant 2 mm or 3 mm larger than the last reamer.

Acetabulum↗
PubMed1992

Tibiotalar contact and fibular malunion in ankle fractures. A cadaver study.

Six cadaveric ankles were dissected, preserving medial and lateral ligaments; an axial load of 455N was applied to the tibia supported by the foot and ankle. The unconstrained tibia was moved through 20 degrees of flexion and extension to simulate walking. The tibiotalar contact area was defined using carbon black suspension, recorded photographically, and measured using computerized area analysis. Osteotomy of the distal fibula was performed and fixed with a specially modified plate; a selection of plates provided fixation with 0 degrees or 30 degrees of external rotation in combination with 0 or 2 mm of shortening. The contact area was measured for each of the plates and after division of the deltoid ligament. There were greater than 30 percent decreases in tibiotalar contact with both fibular shortening and external rotation, doubled with a divided deltoid ligament. Anatomic restoration of both fibular length and rotation is essential for normal ankle mechanics. The deltoid ligament has crucial effects on the stability of the ankle mortise.

Ankle Joint↗
PubMed1992

Left main coronary artery dissection during cardiac catheterization.

A 70-year-old man with a downward sloping origin of the left main coronary artery developed left main dissection at coronary angiography and died despite emergency coronary by-pass surgery. Autopsy showed that the left main coronary artery had an acute angle take off and dissection had originated at the junction of the superior wall of the left main and the aorta. The combination of left main stenosis secondary to dissection and severe right coronary atherosclerosis had caused circumferential subendocardial left ventricular infarction. The left main coronary artery had mild atherosclerosis and lacked cystic medial necrosis. An angulated left main coronary artery may be a risk factor for dissection at angiography.

Aged↗
PubMed1992

The Ring total knee replacement--a comparison of survivorship.

Long term results of joint replacement are frequently expressed as survivorship; it therefore becomes increasingly important to have the ability to make valid comparisons between survivorship tables in order to determine accurately the statistical significance of published differences. We present a statistical method for direct comparison of survivorship tables. We have applied this technique to evaluate the survivorship of the unconstrained, uncemented Ring total knee replacement first implanted in 1975 and compare this to contemporaneous constrained prostheses. There is a significant improvement in survival, which suggests a beneficial long-term effect on the bone/implant interface of this changing design concept.

Aged↗
PubMed1991

Torsades de pointes: arrhythmia, syndrome, or chimera? A perspective in the light of the Lambeth Conventions.

What is torsades de pointes? Is it an arrhythmia or a syndrome? The distinction is critical. In this article I have attempted to explain why this is so. Both from the clinical and nonclinical standpoint, it is of overriding importance that torsades de pointes be amenable to measurement and quantification. This is the fundamental prerequisite for any variable to be of value as an endpoint in an investigation. Measurement and quantification require that a variable has an objective definition that is both inclusive and exclusive. In his seminal work, Dessertenne coined the term torsades de pointes to describe an arrhythmia with unusual features. However, torsades de pointes has been reinterpreted and redefined by Dessertenne's successors. It was originally described as occurring in certain settings (e.g., hypokalemia). However, this has been reinterpreted to mean that a specific set of antecedent conditions (such as hypokalemia) are part of the definition of torsades de pointes. If this is the case, then torsades de pointes is a syndrome, not an arrhythmia. For those more concerned with arrhythmias than with syndromes, the key issue to be determined is what to call the arrhythmia that is part of the syndrome. I have put forward some suggestions with the objective of answering this question, using the Lambeth Conventions as a guide. I believe that there is strong case for ventricular tachyarrhythmias to be classified simply as tachycardia or fibrillation, with the optional use of the term delayed repolarization syndrome in cases where a long QT interval is present. The latter term should be used as one might use the term acute myocardial ischemia, i.e., to denote an underlying condition; it should not be used to define the arrhythmia itself. Twenty-four years after its introduction, the term torsades de pointes has now become a chimera and is best abandoned.

Animals↗
PubMed1991

Evaluation of acetabular stability in uncemented prostheses.

The stability of two commonly used uncemented acetabular prostheses fixed with either pegs or screws has been established by evaluating the torque strengths in ten cadaveric acetabulae. The initial stability of implants to simulated frictional loads was satisfactory compared to previous estimations of the frictional torques in polyethylene-on-metal and metal-on-metal articulations. Testing of the torque required to produce 2 degrees of rotation at the bone-implant interface showed that the peg fixation required significantly greater loads than did the screw fixation (P less than .03). Testing the prostheses to failure gave good results, although lower than previous cemented arthroplasty estimations. The margin of stability over the frictional torques that can be generated is such that it may affect the bony ingrowth into these prostheses. This may account for the common finding of fibrous ingrowth in these prostheses.

Acetabulum↗
PubMed1991

The rabbit dual coronary perfusion model: a new method for assessing the pathological relevance of individual products of the ischaemic milieu: role of potassium in arrhythmogenesis.

STUDY OBJECTIVE: The aim was to develop a new model for determining which factors associated with ischaemia and reperfusion are sufficient for arrhythmogenesis, and to use the model for examining regional hyperkalaemia and K+ washout. DESIGN AND EXPERIMENTAL MATERIAL: Rabbit hearts (n = 150) were perfused with a buffered solution containing K+ in the normal range (2,3,4, or 5 mM). The circumflex coronary artery was perfused independently with a similar solution at a similar rate. A regional increase in K+ concentration was produced, followed by restoration of control K+ to mimic regional changes in K+ during ischaemia and reperfusion. MEASUREMENTS AND MAIN RESULTS: Regional hyperkalaemia (K+ = 9, 12, 15, or 18 mM) mimicked (concentration dependently) the known effects of regional ischaemia on the ECG in three important respects, producing ventricular arrhythmias, regional changes in ECG configuration, and regional alternans. The relationship between arrhythmias and K+ was bell shaped with a peak in susceptibility at 15 mM K+. Arrhythmia susceptibility was reduced and onset delayed by raising the K+ concentration delivered to the adjacent coronary bed. Arrhythmogenesis could be replicated in five or more successive runs in a single heart, indicating a lack of preconditioning. Readmission of control K+ (washout of high K+) mimicked the effects of reperfusion by rapidly causing new episodes of ventricular arrhythmias. The concentration dependence of this effect was exponential, not bell shaped, with washout of 18 mM K+ most arrhythmogenic. There was no preconditioning phenomenon. CONCLUSIONS: Regional hyperkalaemia and K+ washout are factors sufficient to account for arrhythmogenesis during ischaemia and reperfusion, respectively. The new model is suitable for assessment of whether these factors are also necessary for arrhythmogenesis (by equivalent evaluation of other putative arrhythmogens).

Animals↗
PubMed1991

Influence of tedisamil on the initiation and maintenance of ventricular fibrillation: chemical defibrillation by Ito blockade?

We examined the effects of tedisamil on ventricular fibrillation (VF) elicited by regional ischemia and by reperfusion in isolated rat hearts (n = 12/group). During 30 min of ischemia, 0.1, 0.55, and 3 microM tedisamil had no influence on the incidence of VF (an index of VF initiation). However, sustained VF (SVF, defined as that lasting greater than 120 s, an index of VF maintenance) was reduced in a concentration-dependent manner from 73 to 54, 17 (p less than 0.05), and 0% (p less than 0.05), respectively. Tedisamil caused sinus bradycardia but this was not the basis for tedisamil's antiarrhythmic activity since SVF was also inhibited in separate groups of hearts that were paced throughout the study. Tedisamil had no effect on reperfusion-induced VF initiation. However, VF maintenance was, again, inhibited, with SVF incidence reduced from 75% to 40, 20, and 0% (p less than 0.05), respectively, by increasing concentrations of tedisamil. A similar effect was, again, observed in paced hearts. The average cycle length of the electrogram during VF correlated with preceding width of the ventricular complex; both of these variables were concentration-dependently increased by tedisamil and mean values of each correlated inversely with the incidence of SVF. The ratio of SVF cycle length to ventricular tachycardia cycle length was 1:3, and this ratio was conserved in the presence and absence of drug. The data are consistent with a drug-induced increase in the probability of spontaneous termination of multiple wave-front re-entry.

Action Potentials↗
PubMed1991

Independent dual perfusion of left and right coronary arteries in isolated rat hearts.

A novel dual lumen aortic cannula was designed and constructed to permit independent perfusion of left and right coronary beds in isolated rat hearts without necessitating the cannulation of individual arteries. Stability of the dual-perfusion preparation was shown to be similar to that of the conventional Langendorff preparation, in terms of coronary flow, heart rate, and high-energy phosphate content. The independence of left and right perfusion beds was confirmed by unilateral infusion of disulfine blue dye and spectrophotometric detection of the dye in ventricular homogenates. Transient cessation of flow to the left coronary bed resulted in severe ventricular arrhythmias upon reperfusion, as in conventional models of regional ischemia and reperfusion. The dual-perfusion model is technically undemanding, reproducible, inexpensive, and can be used in several species. It enables studies with 1) regional low flow ischemia, 2) regional zero-flow ischemia without coronary ligation (with attendant damage to vasculature), 3) selective application of drugs or interventions to the ischemic-reperfused zone, and 4) selective application of components of ischemia and reperfusion to a site anatomically relevant to ischemic heart disease.

Animals↗
PubMed1991

The pathophysiological basis of arrhythmogenesis in myocardial ischemia and reperfusion: possible target for intervention.

Regional ischemia and reperfusion alter the homeostasis of many substances in the myocardium. Which, if any play a role as pathophysiological progenitors of the associated arrhythmias? The key questions which must be answered in relation to each are: (i) is the presence of the substance sufficient to account for arrhythmogenesis and (ii) is the presence of the substance necessary for arrhythmogenesis to occur? Although there are many candidates for the role of pathophysiological progenitor, and although there is much evidence in support of a role for various of these, the evidence is largely circumstantial. Some of this evidence is reviewed here. I am of the view that new models must be developed if unequivocal data are to be derived. An example which may be of value in this regard is the newly developed rabbit dual perfusion model. The technical aspects of this model are described herein. Using this model I have examined the role of one prospective pathophysiological progenitor of arrhythmogenesis, K+, the intra-extracellular homeostasis of which is disturbed by ischemia and reperfusion in a manner related on a temporal basis with development of susceptibility to arrhythmogenesis. The article concludes with some speculation on possible future research directions.

Angiotensin II↗
PubMed1990

Are reperfusion-induced arrhythmias caused by disinhibition of an arrhythmogenic component of ischemia?

Isolated rat hearts were used to examine whether reperfusion-induced arrhythmias may be caused by washout of substances accumulating during ischemia. This was achieved by subjecting hearts to 10 min of regional ischemia and rendering them transiently inexcitable during the first 1.5 min of reperfusion. Transient inexcitability was induced by switching to cold solution (4 degrees C) shortly before reperfusion (-1.5 min). In controls (no hypothermia), the incidences of ventricular tachycardia (VT) and ventricular fibrillation (VF) were 83% and 92%, respectively, during the first 1.5 min of reperfusion. Transient hypothermia caused inexcitability and asystole, impaired recovery of coronary flow and abolished VT and VF (all P less than 0.05). On subsequent rewarming to 37 degrees C, coronary flow and sinus rate recovered in all hearts. However, VT and VF occurred in only 58% and 25%, respectively (P less than 0.05). These values were similar to those of new episodes of VT and VF occurring in controls during the equivalent period. Therefore arrhythmias had been abolished during transient hypothermia, not merely delayed. The relative contributions of transient impairment of recovery of coronary flow and transient asystole to the antiarrhythmic effects were examined in a further 10 groups of hearts (n = 12/group) in which reperfusion conditions were transiently manipulated. We utilized combinations of hypothermia, ventricular pacing, acetylcholine (ACh) 55 microM (to cause asystole and impairment of recovery of coronary flow), and right atrial excision and left atrial pacing (to permit bradycardia to be transiently induced during reperfusion by temporarily switching off the pacemaker). The results indicated that transient hypothermia was antiarrhythmic as a result of a reduction of excitability, not because of bradycardia or impairment of recovery of flow. The data support the hypothesis that reperfusion unmasks (disinhibits) latent arrhythmogenic components of ischemia (particularly during the first 1.5 min of reperfusion) and that, by inducing inexcitability, transient hypothermia allows these substances to be washed out without their arrhythmogenic effects being manifested. The identities of the arrhythmogenic and antiarrhythmic substances remain to be determined; we suggest that cyclic AMP and potassium, respectively, are likely candidates.

Acetylcholine↗
PubMed1990

Reperfusion and readmission of oxygen. Pathophysiological relevance of oxygen-derived free radicals to arrhythmogenesis.

We have examined the pathophysiological role of readmission of oxygen (and hence production of oxygen-derived free radicals) in the initiation of reperfusion-induced arrhythmias by separating, on a temporal basis, readmission flow from readmission of oxygen. Isolated rat hearts (n = 12/group) were subjected to 10 minutes of regional ischemia and 10 minutes of reperfusion. In controls reperfused with oxygenated solution (Po2 greater than 600 mm Hg), 92% of hearts developed ventricular fibrillation (VF) during the first 20 seconds of reperfusion, whereas in hearts reperfused with hypoxic solution (Po2 9.3-12.2 mm Hg), the incidence of VF was only 17% (p less than 0.05). Subsequent readmission of control solution (Po2 greater than 600 mm Hg) to the latter group led, within 20 seconds, to the appearance of VF in seven of the 10 hearts (70%) that had not previously fibrillated. To examine whether hypoxic reperfusion had prevented VF or merely delayed its onset, the studies were repeated in separate groups of hearts with the duration of hypoxic reperfusion extended to 5 minutes. In addition, to examine the partial pressure dependence of the relation, the Po2 in the reperfusion solution was set at one of five different levels: greater than 600, 150-192.7, 69-85.6, 9.2-14.8, or 0.0 mm Hg. It was found that hypoxia merely delayed VF onset by 20-40 seconds and did not significantly reduce the incidence of VF, which was 83%, 92%, 67%, 58%, and 58%, respectively. This indicated that readmission of oxygen is unnecessary for the initiation of VF during reperfusion. The hearts that reverted to sinus rhythm during the ensuing 5 minutes (n = 8, 4, 5, 9, and 8, respectively) were used to assess the arrhythmogenic consequences of readmission of oxygen. When control solution (Po2 greater than 600 mm Hg) was readmitted, new episodes of VF were elicited within 20 seconds in a manner that was inversely proportional to the preceding Po2 (p less than 0.05), the incidence of new episodes of VF being 0%, 0%, 40%, 67%, and 86%, respectively. The arrhythmogenic effect of readmission of oxygen was not the result of a sudden increase in heart rate, because a similar arrhythmogenic effect of readmission of oxygen was seen in separate groups of hearts that were paced (350 beats/min) throughout hypoxia and readmission of oxygen. In conclusion, readmission of flow and readmission of oxygen are independent determinants of reperfusion-induced arrhythmias.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗