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Biomedical subjects

J E Flack

Publications and source records attributed to J E Flack.

18 recordsLinked to original sources
PubMed1995

Drug-induced heat-shock preconditioning improves postischemic ventricular recovery after cardiopulmonary bypass.

BACKGROUND: Heat-stress preconditioning of mammalian heart has been found to confer protection against ischemic reperfusion injury. Heat shock is generally provided by warming the animal by mechanical means, which is often impractical in a clinical setting. Amphetamine, a sympathomimetic drug, can elevate the body temperature as a result of enhanced endogenous lipolysis. In this study, we examined the effects of heat shock induced by amphetamine on postischemic myocardial recovery in a setting of coronary revascularization for acute myocardial infarction. METHODS AND RESULTS: Adult Yorkshire swine were injected with amphetamine (3 mg/kg IM) (n = 12), and body temperature was continuously monitored. For control studies, the pigs were injected with saline (n = 12). Five swine in each group were killed after 3 hours to obtain biopsies of vital organs to measure heat-shock protein (HSP) mRNAs. After 40 hours, the remaining 7 pigs in each group were placed on cardiopulmonary bypass, and the isolated, in situ heart preparations were subjected to 1 hour of occlusion of the left anterior descending coronary artery followed by 1 hour of global hypothermic cardioplegic arrest and 1 hour of reperfusion. Postischemic myocardial performance was monitored by measuring left ventricular (LV) pressure, its dP/dt, myocardial segment shortening, and coronary blood flow. Cellular injury was examined by measurement of creatine kinase release. The antioxidant enzymes superoxide dismutase and catalase were also assayed. Amphetamine treatment was associated with the induction of mRNAs for HSP 27, HSP 70, and HSP 89 in all the vital organs, including heart, lung, liver, kidney, and brain. Amphetamine also enhanced superoxide dismutase and catalase activities in the heart. Significantly greater recovery of LV contractile functions was noticed, as demonstrated by improved recovery of LV developed pressure (61% versus 52%), LV dP/dtmax (52% versus 44%), and segment shortening (46.2% versus 10%) and reduced creatine kinase release in the amphetamine group. CONCLUSIONS: The results demonstrate that amphetamine can induce whole-body heat shock that can precondition the heart, enhancing cellular tolerance to ischemia-reperfusion injury. Amphetamine is a sympathomimetic drug that may be used for preconditioning.

Amphetamine↗
PubMed1995

Improved 4- and 6-hour myocardial preservation by hypoxic preconditioning.

BACKGROUND: A brief hypoxic episode can precondition myocardium against a subsequent ischemic-reperfusion injury. The present study sought to determine whether intracellular ionic alterations, induced expression of heat-shock proteins (hsps), and/or catalase are involved in the cellular mechanisms by which hypoxic preconditioning can preserve postischemic function in a model of prolonged hypothermic storage. METHODS AND RESULTS: Two groups of isolated working rat hearts were studied: control (CON) and hypoxically preconditioned (HP) hearts. Hearts were arrested at 4 degrees C with St Thomas' cardioplegic solution and immersion-stored for either a 4- or 6-hour period. Myocardial function (ie, heart rate, aortic flow, coronary flow, developed pressure, and its first derivative dP/dtmax) was determined at baseline, after preconditioning, and during reperfusion. At similar time points, myocardial [Na+]i, [K+]i, [Mg2+]i, and [Ca2+]i were measured using an atomic absorption spectrophotometer, and the induction of hsp 70 and catalase mRNAs was assayed using Northern blot analysis. After 4 and 6 hours of hypothermic storage, aortic flow, dP/dtmax, and [K+]i were increased, whereas [Na+]i and [Ca2+]i were decreased significantly in the HP group compared with the CON group. Steady state mRNA levels of catalase and hsp 70 were increased from baseline levels only in the HP group, with a peak (2.8- and 2.4-fold versus baseline) after 4 hours of storage. CONCLUSIONS: Our results indicate that intracellular ionic alterations and upregulation of catalase and hsp 70 gene expression may contribute to the mechanisms underlying hypoxic preconditioning, leading to improved postischemic function during prolonged hypothermic storage of hearts.

Animals↗
PubMed1995

Hypoxic preconditioning enhances functional recovery after prolonged cardioplegic arrest.

The purpose of this study was to assess the ability of hypoxic preconditioning to improve myocardial salvage after prolonged hypothermic cardioplegic arrest. Isolated working rat hearts were arrested at 4 degrees C with St. Thomas' Hospital cardioplegic solution and immersion stored for 4 or 6 hours. Two groups were studied, control and hypoxically preconditioned (HP) hearts. After 4 hours' preservation, aortic flow, coronary flow, and the first derivative of aortic pressure were 8.7 +/- 1.6 mL/min, 17.8 +/- 1.6 mL/min, and 2,064 +/- 123 mm Hg/s, respectively, in control hearts (n = 11) and 25.7 +/- 2.5 mL/min, 27.1 +/- 2.5 mL/min, and 2,655 +/- 93 mm Hg/s, respectively, in HP hearts (n = 11) (p < 0.05). After 6 hours' preservation, aortic flow, coronary flow, and the first derivative of aortic pressure were 3.5 +/- 1.2 mL/min, 18.8 +/- 0.4 mL/min, and 1,622 +/- 226 mm Hg/s, respectively, in control hearts (n = 6) and 21.5 +/- 3.2 mL/min, 25.5 +/- 2.3 mL/min, and 2,439 +/- 239 mm Hg/s, respectively, in HP hearts (n = 6) (p < 0.05). After 6 hours' preservation, adenine nucleotides and creatine phosphate levels were not significantly different between the two groups, but lactate dehydrogenase release was significantly increased (p < 0.05) in control versus HP hearts (4.66 +/- 0.58 IU/L versus 1.98 +/- 0.28 IU/L). We conclude that hypoxic preconditioning reduces cellular necrosis and preserves myocardial function after prolonged hypothermic cardioplegic arrest.

Adenine Nucleotides↗
PubMed1995

Tranexamic acid significantly reduces blood loss associated with coronary revascularization.

Four hundred fifteen patients undergoing coronary revascularization over a 12-month period were divided into two groups: 209 controls in the first 6 months received no tranexamic acid (TA) before cardiopulmonary bypass and 206 patients in the second 6 months received TA as a hemostatic agent. The demographics and the surgical techniques used were similar in the two groups. With TA there was a significant decrease in blood loss postoperatively, from 1,114.1 mL in the controls to 803.7 mL in those given TA (p < 0.001); in red blood cell use, from 1.7 units/patient in the controls to 0.69 units/patient in those given TA (p < 0.001); in fresh frozen plasma requirements, from 0.23 units/patient in the controls to 0.024 units/patient in those given TA (p < 0.01); and in platelet transfusion, from 1.06 units/patient in the controls to 0.30 units/patients in those given TA (p < 0.01). The percentages of patients not receiving any blood products were 65% in those given TA versus 49% in the controls (p < 0.01). There was no significant difference between the two groups in the incidence of perioperative myocardial infarction, cerebrovascular accidents, pulmonary embolism, or venous thrombosis to clearly suggest hypercoagulability. In this study, TA profoundly affected the coagulopathy associated with bypass in patients undergoing coronary revascularization. It significantly reduced blood loss and blood product transfusions. Any potential increased thrombotic complications could not be clearly demonstrated in this study, but should not be ignored.

Aged↗
PubMed1995

Influence of steroids on complement and cytokine generation after cardiopulmonary bypass.

BACKGROUND: It is recognized that the inflammatory mediators complement and cytokines are generated during cardiopulmonary bypass as an endogenous response to extracorporeal circulation. METHODS: Nineteen randomized patients (10 steroid/9 nonsteroid) entered an institutional review board-approved protocol to measure complement and interleukin level generation before and after elective coronary revascularization. The steroid regimen involved 1 g of methylprednisolone sodium succinate intravenously before bypass and 4 mg of dexamethasone every 6 hours for four doses during the first 24 hours of recovery. Complement and interleukin levels were measured before bypass, immediately after bypass, and at 24, 48 and 72 hours of recovery. RESULTS: In the nonsteroid group, there was a significant elevation in all inflammatory mediators relative to the steroid group. The predominant changes occurred at 24 hours after operation. CONCLUSIONS: Steroids produced a dramatic reduction in complement and interleukin levels. The number of patients was clearly too small to document a clinical consequence of steroid administration.

Aged↗
PubMed1995

Constitutive nitric oxide release is impaired after ischemia and reperfusion.

Myocardial ischemia and reperfusion may result in endothelial dysfunction and reduced release of nitric oxide. With the use of an amperometric sensor, the first direct measurements of constitutive nitric oxide release from a beating heart were measured from the coronary effluent of isolated working rat hearts subjected to ischemia and reperfusion. Rats, six to eight per group, were randomly studied as follows: control (no pretreatment) and pretreatment with the nitric oxide donor L-arginine (3 mmol/L), its enantiomer D-arginine (3 mmol/L), nitric oxide inhibitor N omega-nitro-L-arginine methyl ester (100 mumol/L), and combined N omega-nitro-L-arginine methyl ester/L-arginine. Isolated hearts were pretreated for 10 minutes before 30 minutes of global ischemia and 30 minutes of reperfusion. A nonischemic control group (n = 4) was continuously perfused with oxygenated unsupplemented buffer. After ischemia/reperfusion, hearts supplemented with L-arginine recovered significantly (p < 0.05) increased developed pressure, first derivative of the aortic pressure (dP/dtmax), and aortic flow compared with all other hearts that underwent ischemia/reperfusion. In addition, nitric oxide release was significantly (p < 0.05) increased during reperfusion in the L-arginine group. During reperfusion, the recovery of aortic flow correlated with nitric oxide release (r = 0.81, p < 0.0001). We conclude that after ischemia/reperfusion, endothelial dysfunction results in decreased nitric oxide release, which can be ameliorated with L-arginine pretreatment. The direct cytoprotective properties of nitric oxide may contribute to improved functional recovery in hearts pretreated with L-arginine. Augmentation of the L-arginine/nitric oxide pathway may provide a new approach for improved recovery after cardiovascular operations.

Animals↗
PubMed1995

Does cardiopulmonary bypass temperature correlate with postoperative central nervous system dysfunction?

A National Institutes of Health-funded trial of perfusate temperature and neurological function was begun in the Baystate Medical Center in February 1994. It randomizes patients having coronary revascularization to three temperatures--warm (37 degrees C), tepid (32 degrees C), and cold (20 degrees C)--for systemic perfusate and blood cardioplegia temperature at 37 degrees C warm, 32 degrees C tepid, and 6 degrees C to 10 degrees C cold. The goal is to have a quantitated neurological examination performed prior to operation, prior to discharge at day 3 or 4, and at a 1-month follow-up interval. The initial 51 patients completing a 1-month follow-up broke down to 14 cold, 22 tepid, and 15 warm. The neurological examination quantitated their performance on the Mathew Scale, an ordinal measure from 1 to 100, with 100 being normal. There was a significant (p < 0.05) decrease across the entire study from preoperative to postoperative that was no longer present at late follow-up. Although the lowest mean scores (94.8) occurred in the warm group, they were not statistically different from the other groups', and there was no discernible influence of temperature on neurological function. Additional patients will be entered to validate a difference if such exists.

Aged↗
PubMed1994

Fast-track recovery of the coronary bypass patient.

A new approach termed "fast-track recovery" ws undertaken at both the Baystate Medical Center and Hartford Hospital. The fast-track protocol involves the following principles: (1) preoperative education; (2) early extubation; (3) methylprednisolone sodium succinate before bypass followed by dexamethasone for 24 hours postoperatively; (4) prophylactic digitalization, metoclopramide HCl, docusate sodium, and ranitidine HCl; (5) accelerated rehabilitation; (6) early discharge; (7) a dedicated fast-track coordinator to perform both daily telephone contact and a 1-week postoperative examination; and (8) a routine 1-month postoperative visit with a PA or MD. To evaluate the effects of this approach on patient care, a retrospective 1-year analysis was undertaken in both institutions with all coronary artery bypass grafting patients compared in a consecutive manner before the origin of the fast-track protocol and subsequent to its beginning. There were 280 patients in the fast-track and 282 in the non-fast-track group. The two groups were not significantly different except inexplicably there was a lower ejection fraction in the fast-track group and a longer cross-clamp time. Postoperatively, the mean time to extubation decreased from 22.1 to 15.4 hours, and peak weight gain decreased from 2.8 to 1.6 kg from the non-fast-track to the fast-track group (p < 0.01). This was accompanied by significant (p < 0.001) decreases in intensive care unit duration from 2.4 to 1.9 days and in postoperative length of stay from 8.3 to 6.8 days from the non-fast-track to the fast-track group. There was no increase in morbidity or mortality associated with the fast-track protocol either early or late. Thirty-day hospital readmission was not significantly different between the two groups. Fast-track methodology is effective, and we routinely employ this approach for all patients undergoing cardiopulmonary bypass.

Aged↗
PubMed1994

Emergency cardiopulmonary bypass in the cardiac surgical unit can be a lifesaving measure in postoperative cardiac arrest.

BACKGROUND: Postoperative cardiac arrest that is not responsive to conventional resuscitation is uniformly fatal. Sixteen patients who experienced postoperative ventricular fibrillation (VF) and arrest over a 6-year period and did not respond to open chest resuscitation were placed on an emergency basis on cardiopulmonary bypass (CPB) in the cardiac surgical intensive care unit (CSICU). METHODS AND RESULTS: Data were reviewed by retrospective analysis. Nine of the 16 patients (56.3%) survived, and they spent a mean of 9 +/- 2.8 days in the CSICU and a mean of 17 +/- 4.6 days in the hospital. They all are alive 1 month to 5 1/2 years later. The mean interval between VF/arrest and CPB in the CSICU was 50 +/- 6.7 minutes (range, 25 to 83 minutes) for survivors and 51 +/- 6.1 minutes (35 to 83 minutes) for nonsurvivors (P = .98). The duration of CPB in the CSICU was 111 +/- 16.0 minutes (range, 55 to 189 minutes) for survivors and 167 +/- 20.7 minutes (range, 80 to 232 minutes) for nonsurvivors (P = .05). There were no apparent differences between survivors and nonsurvivors in age, history of arrhythmias, use of antiarrhythmics, congestive heart failure, recent myocardial infarction, ejection fraction, preoperative intra-aortic balloon pump, urgency, or type of operation. Surgical variables and postoperative medications and electrolytes (after the primary procedure) were similar. The use of cardioplegic arrest during CPB in the CSICU was higher among survivors (3 of 9) compared with 0 of 7 for nonsurvivors (P = .21). There was no mediastinitis and only two minor soft tissue infections among survivors. CONCLUSIONS: The use of CPB in the CSICU can achieve significant survival in patients who have otherwise irreversible cardiac arrest and/or VF after surgery; the incidence of infection in patients undergoing CPB in the CSICU is very low; and the use of warm cardioplegic arrest may enhance the changes of survival in this type of patient.

Aged↗
PubMed1994

Normothermic cardioplegia prevents intracellular calcium accumulation during cardioplegic arrest and reperfusion.

BACKGROUND: Development of intracellular calcium overloading is to be a primary factor in cellular injury during myocardial reperfusion. We studied the effects of different temperatures during continuously perfused cardioplegic arrest on the changes of intracellular calcium concentration ([Ca2+]i) level in isolated rat hearts. METHODS AND RESULTS: Rat hearts were perfused by the Langendorff technique with Krebs-Henseleit bicarbonate (KHB) buffer. The [Ca2+]i was monitored by loading the heart with fura-2 acetoxymethyl ester and by using a [Ca2+]i analyzer. [Ca2+]i was calculated by determining the maximal and minimal fluorescent intensity for each heart. The hearts (n = 6 in each group) were subjected to cardioplegic arrest by continuous perfusion of oxygenated crystalloid K+ (15 mEq/L) cardioplegic solution (CPS) at different temperatures (4 degrees C, 20 degrees C, 28 degrees C, 37 degrees C) for 120 minutes, followed by 30 minutes of normothermic KHB buffer reperfusion. A fifth group received continuous perfusion as a control with 37 degrees C KHB buffer. The baseline values of [Ca2+]i were comparable in all experimental groups. In hearts perfused with 4 degrees C CPS, [Ca2+]i increased significantly during reperfusion (from 221 +/- 24 nmol/L [mean +/- SEM] at baseline to 341 +/- 19 at the end of reperfusion, P < .05). CPS perfusion at 20 degrees C also induced significant Ca2+ overloading during reperfusion, but not as much as in the 4 degrees C group. No significant [Ca2+]i increase occurred at 28 degrees C or 37 degrees C. CONCLUSIONS: Continuous cardioplegic perfusion at lower temperatures (ie, 4 degrees C or 20 degrees C) induces Ca2+ overloading during reperfusion, which is detrimental to the optimal recovery of ventricular performance, while normothermic cardioplegic perfusion prevents the development of Ca2+ accumulation. These results provide experimental evidence for a detrimental effect of prolonged hypothermic continuous cardioplegia.

Animals↗
PubMed1992

Heat shock. A new approach for myocardial preservation in cardiac surgery.

BACKGROUND: Recent studies have indicated that heat shock (HS) induces protective genes and HS protein (HSP) expression, which enhances cellular tolerance to ischemic injury. The present study sought to determine if 42 degrees C blood cardioplegia could be used to induce HSP expression and improved myocardial salvage after 2 hours of cardioplegic arrest. METHODS AND RESULTS: To study this, pig hearts (n = 6) on cardiopulmonary bypass were subjected to HS by continuous infusion to the globally arrested heart of warm blood cardioplegia (K+ = 30 meq/l) at 42 degrees C for 15 minutes followed by 2 hours of intermittent hypothermic (4-6 degrees C) hyperkalemic (30 meq/l) crystalloid cardioplegic arrest and 1 hour of reperfusion (heat shock group). The control group (n = 6) was subjected to only 2 hours of hypothermic crystalloid cardioplegic arrest followed by 1 hour of reperfusion without HS. Left ventricular performance, coronary blood flow, and creatine kinase release were determined before arrest and during reperfusion. Prearrest control biopsies were taken in a separate group of pigs (n = 6) for both HSP and superoxide dismutase activity. Additional biopsies were taken for the same measurements in both control and HS groups at the completion of reperfusion. In a single additional pig in both the control and HS groups, biopsies were taken during the study to estimate changes in HSP expression. The cytosolic protein of ventricular tissue was subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and the HSP70 family protein was examined by Western blot analysis using monoclonal antibodies. HSP was found to be increasingly expressed from control levels after 15 minutes of HS pretreatment, increasing progressively to a level significantly above the non-HS group. Associated with this increased expression of HSP was a significant increase in superoxide dismutase activity in the HS animals and significant improvement in both global and regional functions and reduced creatine kinase release. CONCLUSIONS: The results show that preconditioning the heart with HS improves postischemic ventricular performance and attenuates cellular injury. HS induces a change in cellular metabolism, prompting the expression of HSP and improving antioxidant activity, leading to improved function and reduced tissue injury during ischemia and reperfusion.

Animals↗
PubMed1992

Effect of normothermic blood cardioplegia on postoperative conduction abnormalities and supraventricular arrhythmias.

BACKGROUND: Conduction defects and supraventricular tachycardia (SVT) are common after myocardial revascularization using current methods of cold hyperkalemic blood or crystalloid cardioplegia. The current retrospective study was undertaken to assess the influence of normothermic blood cardioplegia on conduction defects and SVT. METHODS AND RESULTS: The initial 92 patients underwent cardiopulmonary bypass (CPB) at 28 degrees C and blood cardioplegia at 6-8 degrees C. The subsequent 120 patients underwent CPB and blood cardioplegia at 37 degrees C. In all patients, cardioplegia was initially given by a combined antegrade/retrograde technique. The incidence of new postoperative conduction disturbances was significantly less in the normothermic group (p < 0.001): 27.5% versus 57.6% immediately after surgery; 9.2% versus 41.3% 1 day after surgery; 4.2% versus 32.6% 2 days after surgery; 1.7% versus 19.6% on hospital discharge; and 1.7% versus 17.4% on late follow-up. The incidence of supraventricular arrhythmias was not statistically different: 40.0% warm versus 42.4% cold. The groups were identical except that mean cross-clamp times were significantly longer (73.8 versus 60.1 minutes), mean number of grafts were significantly higher (3.7 versus 3.4), and mean cardioplegia volume was significantly greater (5,627 versus 3,710 ml) in the warm group (p < 0.05). In addition, the warm group had a higher incidence of prior transmural anterior myocardial infarctions (35% versus 9.8%, p < 0.001) and emergency operation (16.7% versus 6.5%, p < 0.05). Creatine kinase (CK) MB release was significantly less in the warm group immediately after operation (24.9 versus 60.9 units/l) and on POD1 (19.2 versus 46.5 units/l) (p < 0.001). CONCLUSIONS: Normothermic cardioplegia is associated with a marked decrease in new and permanent conduction disturbances and postoperative CK-MB release. This suggests that a significant factor in the pathogenesis of conduction blocks is cold-related injury. Supraventricular arrhythmias were not affected by the type of cardioplegia given.

Blood↗
PubMed1991

Cardiac retractor for coronary bypass operations.

The Thompson retractor, used mainly for abdominal procedures, has been used to retract the heart and facilitate exposure for the performance of inferior wall or posterolateral wall coronary anastomoses. It has been found to be very effective and can replace a second assistant to retract the heart or avoid other cumbersome methods of cardiac retraction.

Coronary Artery Bypass↗
PubMed1991

Reduction of infarct size by systemic amino acid supplementation during reperfusion.

The amino acids aspartate and glutamate, in combination, were evaluated as a means of reducing infarct size and improving cardiac function during reperfusion in an intact pig having an acute anteroseptal infarct. Three groups of 6 pigs each were randomly studied in a blinded manner: control (no amino acids), aspartate/glutamate 3 mmol/L, and aspartate/glutamate 13 mmol/L. The left anterior descending coronary artery was occluded distal to its first diagonal branch for 60 minutes followed by reperfusion for 6 hours. Aspartate and glutamate were administered systemically immediately before reperfusion. The following parameters were measured: infarct size and percent area at risk, global metabolic function, global and regional myocardial function, and tissue parameters of metabolic function. The results clearly showed a significant decrease in infarct size from 60% of the area at risk in control pigs to 37% in both 3 mmol/L and 13 mmol/L amino acid groups. Cardiac output, coronary blood flow, and global oxygen consumption were not significantly affected by the use of amino acids relative to the control group. Global left ventricular mechanical function was also not adversely affected by the infarct and was not altered by amino acid administration. Regional function, however, was significantly decreased by occlusion of the left anterior descending coronary artery in all groups to near 20% and only significantly recovered to 64% in the 13 mmol/L amino acid group. Adenosine triphosphate and acetyl coenzyme A measurements documented significant increases in the 13 mmol/L amino acid group relative to the control group. The conclusions of this study strongly support aspartate/glutamate supplementation for stunned, reperfused myocardium. It is apparent that the effect of amino acid supplementation on glycolysis is directly translated into improved regional function and reduced infarct size.

Animals↗
PubMed1991

Preconditioning the heart by repeated stunning improves myocardial salvage.

Repeated regional ischemia of short duration followed by reperfusion leads to preconditioning of the myocardium. Left anterior descending coronary artery (LAD) occlusion was applied for 5 minutes and then released for 10 minutes. This was repeated four times by using an intact pig model. LAD occlusion was then continuously applied for 1 hour. Myocardial function, high energy phosphates, and membrane phospholipids were compared with a control (nonstunned) group over a 6-hour reperfusion period. Stunning itself produced no significant change in regional function, total phospholipids, or free fatty acids (FFA). However, regional function, adenosine triphosphate, and creatine phosphate were significantly (p less than 0.05) reduced over control. After 60 minutes of ischemia, regional function was significantly improved by preconditioning that persisted throughout reperfusion (p less than 0.01). This was associated with an 11% mean decrease in infarct size (p less than 0.05). Adenosine triphosphate was significantly preserved during ischemia in the preconditioned hearts, and this preservation persisted throughout reperfusion (p less than 0.05). Total phospholipids were not affected by ischemia in either group. However, during reperfusion both groups demonstrated a 15-20% decrease in phospholipid levels at 1 hour, with only the stunned group showing a progressive increase at 3 and 6 hours (p less than 0.05). Examination of FFA during reperfusion demonstrated a profound increase in only the unstunned animals (p less than 0.05), correlating with the decreased level of membrane phospholipids noted in this group. In conclusion, repeated stunning predisposes the heart to recovery after regional ischemia. This results in improved mechanical function, increased high-energy phosphate stores, and decreased infarct size.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMedDate not supplied

A comprehensive cardiovascular waveform analysis program for IBM-compatible personal computers.

Computerized cardiovascular waveform processing has become a necessary and fundamental tool in the analysis of physiologic data. The availability of numerous commercial data-analysis programs has significantly enhanced the efficiency of waveform analysis. Many such programs come with their own programming language, which enables the researcher to create an application program suited to a specific series of calculations. Once written, an application program can significantly increase the efficiency with which data from a specific experiment can be analyzed. However, creating or modifying a program for each new experimental protocol can be time-consuming, especially in the error-detection and verification stages. Single-purpose programs also prove somewhat inflexible to unexpected changes in experimental formats. These problems suggested the need for a more flexible program, but one that is nevertheless specifically suited to the analysis of cardiovascular signals. This need led to the development of a program designed in collaboration with surgeons and physiologists. This program addresses some important analysis problems in cardiovascular research, and allows the user to survey and manipulate cardiovascular waveforms in an intuitive and spontaneous manner.

Algorithms↗