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Biomedical subjects

J R Pepper

Publications and source records attributed to J R Pepper.

At least 37 records · Page 2Linked to original sources
PubMed2001

Scapular insertion of the rabbit latissimus dorsi muscle: gross anatomy and fibre-type composition.

This paper defines the characteristics and significance of the scapular insertion of the latissimus dorsi muscle (LDM) of the rabbit. In a study of the New Zealand White species (n = 10) the scapular insertion was found to be a consistent anatomical feature of the LDM that made up 12.3% (+/-2.3) of the total muscle weight. The fibres arise from the medial aspect of the body of the LDM and run in a caudocranial direction to be inserted into a broad, thin tendon beneath the scapula ridge. This is morphologically different from the scapular component of the human LDM which is a well-recognized but inconsistent feature and consists of no more than a small leash of fibres running around the lower pole of the scapula. The scapular insertion was deeper red in colour than the body of the muscle and fibre-typing demonstrated a mean slow-fibre composition of 49% (+/-2.6) compared to 16% (+/-1.7) for the body of the muscle (p < 0.01). Mapping of the fibre types throughout the remainder of the LDM confirmed that the body of the muscle was of fast phenotype but with significantly more slow fibres in the superomedial segment of the muscle than elsewhere. This region of the muscle contributes mainly to the scapular insertion and it is proposed that this part of the muscle takes on a predominantly postural role in stabilising the scapula during movement of the forelimb.

Adenosine Triphosphatases↗
PubMed2001

Comparison of connexin 43, 40 and 45 expression patterns in the developing human and mouse hearts.

The mouse is currently widely used as a model organism in the analysis of gene function but how developmentally regulated patterns of connexin gene expression in the mouse compare with those in the human is unclear. Here we compare the patterns of connexin expression in the heart during the development of the mouse (from embryonic day 12.5 to 6 weeks postpartum) and the human (at 9 weeks gestation and adult stage). The extent of connexin43 expression in the ventricles progressively increased during development of the mouse heart. The developmental pattern of expression for connexins 40 and 45 in the mouse heart was similar, but not identical, and in the ventricles showed a progressive and preferential expression in the conduction system. In general, these dynamic changes of connexins 43, 40 and 45 during mouse cardiac development appear to be mirrored in the human.

Adult↗
PubMed2000

Hybrid management of coronary artery disease and coarctation of aorta.

The treatment of coarctation of aorta with an additional cardiac lesion in adults remains a difficult surgical challenge. We present here an alternative, two-stage, hybrid approach that combined stent repair of aortic coarctation followed by coronary artery bypass operation in an adult with critical coronary lesions and a poor ventricle. This method may be a potentially useful strategy in reducing the comorbidity of operation to both lesions.

Aortic Coarctation↗
PubMed2000

Oxygenation and perfusion of rabbit tibialis anterior muscle subjected to different patterns of electrical stimulation.

Dual amperometric microelectrodes were used to measure local pO2 and perfusion at multiple sites in the fast-twitch tibialis anterior muscles of anaesthetized rabbits. Six muscles were stimulated continuously at 10, 5, or 2.5 Hz. For all three frequencies, perfusion declined to about 50% of resting levels and recovered after stimulation. These changes corresponded to a rise followed by a fall in extracellular pO2. The highest levels of pO2 were reached during stimulation at 10 Hz. Eight muscles were stimulated tetanically at 100 Hz for 200 ms with duty cycles that were varied between 1.3 and 20.0%. Perfusion rose to 8.7 +/- 2.0 ml s(-1) 100 g(-1) at a duty cycle of 5% and declined with further increases in duty cycle. pO2 was depressed for duty cycles less than 10% but rose above resting levels at higher duty cycles. It is suggested that the paradoxical combination of elevated pO2 and depressed perfusion is attributable to stimulation conditions that exceed the oxygen transport capacity of a fast muscle.

Animals↗
PubMed2000

Release of GM-CSF and G-CSF by human arterial and venous smooth muscle cells: differential regulation by COX-2.

In addition to their traditional contractile function, vascular smooth muscle cells can be stimulated under inflammatory conditions to release a range of potent biological mediators. Indeed, we and others have shown that human vascular smooth muscle release the colony stimulating factors (CSF) granulocyte macrophage-CSF (GM-CSF) and granulocyte-CSF (G-CSF) as well as large amounts of prostaglandins following the induction of cyclo-oxygenase-2 (COX-2), when stimulated with cytokines. Here we demonstrate, for the first time, that co-induced COX-2 activity simultaneously suppresses GM-CSF release and potentiates G-CSF release by human vascular cells. Moreover, the differential regulation of GM-CSF and G-CSF release by COX-2 was mimicked by the prostacyclin (PGI(2)) mimetic, cicaprost. These observations suggest that PGI(2), released following the induction of COX-2, differentially regulates the release of GM-CSF (suppresses) and G-CSF (potentiates) from human vascular cells.

Arteries↗
PubMed2000

Evaluation of patients undergoing lung volume reduction surgery: ancillary information available from computed tomography.

AIM: A number of imaging techniques have been used for the pre-operative assessment of patients for lung volume reduction surgery (LVRS). We evaluated whether data currently acquired from perfusion scintigrams and cine MR of the diaphragm are obtainable from high resolution CT (HRCT) of the thorax. MATERIALS AND METHODS: Thirty patients taking part in a randomized controlled trial of LVRS against maximal medical therapy were evaluated. HRCT examinations (n= 30) were scored for (i) the extent and distribution of emphysema; (ii) the extent of normal pulmonary vasculature; and (iii) diaphragmatic contour, apparent defects and herniation. On scintigraphy, (n= 28), perfusion of the lower thirds of both lungs, as a proportion of total lung perfusion (LZ/T(PERF)), was expressed as a percentage of predicted values (derived from 10 normal control subjects). On cine MR (n= 25) hemidiaphragmatic excursion and coordination were recorded. RESULTS: Extensive emphysema was present on HRCT (60% +/- 13.2%). There was strong correlation between the extent of normal pulmonary vasculature on HRCT and on perfusion scanning (r(s)= 0.85, P< 0.00005). Hemidiaphragmatic incoordination on MR was weakly associated with hemidiaphragmatic eventration on HRCT (P= 0.04). CONCLUSION: The strong correlation between lung perfusion assessed by HRCT and lung perfusion on scintigraphy suggests that perfusion scintigraphy is superfluous in the pre-operative evaluation of patients with emphysema for LVRS.

Adult↗
PubMed2000

Vascular endothelial growth factor release following coronary artery bypass surgery: extracorporeal circulation versus 'beating heart' surgery.

AIMS: The aim of this study was to examine the circulating levels of vascular endothelial growth factor, following coronary artery bypass graft surgery performed using both standard cardiopulmonary bypass or the 'octopus technique' on the beating heart. BACKGROUND: Vascular endothelial growth factor has a number of effects that are beneficial in the setting of coronary artery bypass graft surgery including cardioprotection, potent angiogenic activity and amelioration of intimal hyperplasia. Hypoxia is a powerful stimulator of vascular endothelial growth factor expression yet the ability of ischaemia, occurring during coronary artery bypass graft surgery, to induce vascular endothelial growth factor production is unknown. METHODS AND RESULTS: Serum vascular endothelial growth factor levels were determined in patients undergoing coronary artery bypass graft surgery with standard cardiopulmonary bypass (CPB-CABG group; n=20), with off-pump coronary artery bypass; (OP-CABG; n=12) and in patients undergoing non-cardiac major surgery (n=6). The effect of hypoxia on vascular endothelial growth factor release by neonatal rat cardiac myocytes in vitro was studied. In the CPB-CABG group vascular endothelial growth factor levels were significantly increased to 78.5+/-39.3 and 110.5+/-16.3 pg. microl(-1)8 and 24 h post-operatively, declining to 14.9+/-9.9 pg. microl(-1)by 48 h to pre-operative values (14.4+/-8.6 pg. microl(-1)). Significantly higher vascular endothelial growth factor levels were also present in the OP-CABG group 3, 6 and 24 h post-operatively (levels 136. 6+/-29.3, 143+/-26.12 pg. microl(-1)and 93.5+/-20.1 pg. microl(-1), respectively). However, non-cardiac major surgery did not result in elevated vascular endothelial growth factor levels post-operatively (46.36+/-9.76 vs pre-surgery levels of 26.84+/-6.1 pg. microl(-1)). Either 15 min or 3 h of hypoxia stimulated vascular endothelial growth factor release from neonatal rat cardiac myocytes in vitro. Twenty-four and 48 h post hypoxia, levels of vascular endothelial growth factor were significantly elevated by approximately 17.5- and 48.5-fold respectively. CONCLUSIONS: These data demonstrate myocardial ischaemia secondary to CPB-CABG and OP-CABG to be a potent stimulator of vascular endothelial growth factor production, which may have implications for graft endothelialization and cardiovascular haemodynamics post-operatively.

Animals↗
PubMed2000

Experience of totally implantable venous access devices (TIV ADs) in adults with cystic fibrosis over a 13-year period.

Totally implantable venous intravenous access devices (TIVADs) have an essential role in the frequent delivery of antibiotics in cystic fibrosis (CF) patients. This study at the Royal Brompton Hospital (RBH) reports the experience of TIVADs in patients attending the RBH adult CF unit implanted at the RBH and elsewhere over a 13-year period. The case notes of adult CF patients who had undergone TIVAD insertion were reviewed retrospectively. The patients were divided into those who had the insertion carried out at the RBH and those who had the device inserted elsewhere. All devices were cared for the at the RBH. A total of 115 devices in 74 patients were reviewed. The median duration of function of 109 devices was 1429 days (range 2-3989) or 3.9 years, with a total exposure of 91,188 days or 249.8 years. There was no significant difference between devices inserted at the RBH and those inserted elsewhere (P= 0.59). Thirty-four patients had devices installed without complications. Forty patients had complications in 62 devices. The incidence of complications was 34.5% at the devices inserted at RBH and 73.7% elsewhere (P<0.001). Of the 115 devices, mechanical complications occurred in 42 (36%) with a median time of diagnosis of 373 days (range 1-2554), infectious complications occurred in 16 (14%), with a median time of diagnosis of 413 days (range 40-2556) and symptomatic venous thrombosis occurred in four (3.5%). RBH-inserted devices had significantly fewer mechanical complications (P<0.001) compared with those inserted elsewhere. The group as a whole had fewer infectious complications than in most other reported series. We conclude that TIVADs provide effective and long-term intravenous access and have fewer complications if they are inserted and cared for at a centre with special expertise in their insertion and management.

Adolescent↗
PubMed2000

Cyclooxygenase-2 regulates granulocyte-macrophage colony-stimulating factor, but not interleukin-8, production by human vascular cells: role of cAMP.

Vascular smooth muscle is now recognized as an important site of mediator generation under inflammatory conditions. Indeed, the release of leukocyte activators, such as granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin (IL)-8, by human arterial smooth muscle cells has recently been demonstrated. However, the potential for venous cells to release GM-CSF has not been addressed. We have shown that human vascular smooth muscle cells express the "inflammatory" form of cyclooxygenase (COX), cyclooxygenase-2 (COX-2), when stimulated with cytokines. In some nonvascular cell types, the COX activity has been shown to regulate the release of GM-CSF and IL-8, although the nature of the isoform responsible was not addressed. We show that human venous smooth muscle cells, like their arterial counterparts, release GM-CSF after stimulation with IL-1beta. Similarly, both cell types released IL-8. Under the same conditions, we found that COX-2 activity suppressed GM-CSF, but not IL-8, release by both types of human vascular cells. Moreover, the prostacyclin mimetic, cicaprost, and the cAMP analogue, dibutyryl cAMP, inhibited GM-CSF release from these cells. These observations suggest that COX-2 activity suppresses GM-CSF release via a cAMP-dependent pathway in human vascular cells and illustrates a novel mechanism by which this enzyme can modulate immune and inflammatory events.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2000

Myocardial tissue oxygen supply and utilization during coronary artery bypass surgery: evidence of microvascular no-reflow.

The supply and utilization of oxygen by the myocardium reflect the dynamic efficiency of the microcirculation. The present study examines these parameters during coronary artery bypass surgery. We used a voltammetric microelectrode technique to assess regional variations in myocardial tissue partial pressure of oxygen (PO(2)) and myocardial tissue perfusion (MTP) in patients undergoing coronary artery bypass surgery. A total of 29 myocardial regions were studied in 17 patients to assay tissue PO(2), and 13 regions in 10 patients to measure MTP. There was an increase in MTP from 53+/-9 ml.min(-1).100 g(-1) before cardiopulmonary bypass to 72+/-13 ml. min(-1).100 g(-1) after (means+/-S.E.M.; P=0.05). Tissue PO(2) showed an overall increase from a baseline level of 45+/-8 mmHg to a final level of 88+/-10 mmHg (P<0.0001). Following release of the aortic cross-clamp there was a variable time delay before a change in tissue PO(2) was observed. There was an immediate response in five regions, whereas in 20 regions the response was delayed by between 0.5 and 32 min. In the remaining four regions there was no change in tissue PO(2). The duration of the delay in response was correlated positively with the cross-clamp time (r=0.45, P<0.05) and negatively with the final tissue PO(2) (r=-0.5, P<0.05). Voltammetric methods for monitoring changes in oxygen supply and utilization offer new insights into the changes that occur during ischaemia and reperfusion. A delay in the delivery of oxygen to the myocardium occurs in many patients following coronary artery bypass surgery.

Aged↗
PubMed2000

Tissue factor is rapidly elevated in plasma collected from the pericardial cavity during cardiopulmonary bypass.

There is growing evidence that the tissue factor/factor VIIa pathway of coagulation is enhanced during cardiopulmonary bypass. Hitherto, available evidence has suggested that upregulated monocyte bound tissue factor is made available, either in the blood collected from the site of surgery or on circulating cells. However, cellular upregulation is slow, while generation of factor VIIa in blood collected from the pericardial cavity is rapid. We have therefore investigated the possibility of an alternative source of tissue factor, plasma (as opposed to cellular) tissue factor in blood samples taken from the central vein catheter (systemic circulation) and collected from the pericardial cavity during cardiopulmonary bypass. Six patients undergoing first time cardiopulmonary bypass grafting were studied. Tissue factor antigen was found to be rapidly elevated (by 15 min) in the pericardial plasma, approximately 5-fold above systemic levels (p <0.004). Similar elevations were found in markers of coagulation activation, factor VIIa antigen (p = 0.066), prothrombin fragment F(1+2) (p <0.003) and thrombin-antithrombin complex (p <0.03). To explore whether plasma tissue factor was (or had been) functionally active, factor VIIa was measured also with the soluble tissue factor functional assay after removal of heparin. Functional factor VIIa activity fell significantly in the systemic circulation, probably due to the heparin-induced increase (approximately 15-fold) in tissue factor pathway inhibitor (TFPI), but was elevated in pericardial blood compared with that taken from the central line catheter (p <0.006). These results demonstrate that both components of the activation complex for the extrinsic pathway of coagulation are rapidly generated in pericardial blood during bypass.

Aged↗
PubMed1999

Valve replacement for aortic stenosis in patients with poor left ventricular function: comparison of early changes with stented and stentless valves.

BACKGROUND: Long-standing aortic stenosis causes significant left ventricular (LV) dysfunction, which may progress irreversibly. In many cases, LV function can be salvaged by aortic valve surgery, although debate exists regarding the best valve prosthesis to use. METHODS AND RESULTS: We studied 33 patients retrospectively who had significant aortic stenosis and impaired LV systolic function, as assessed by transthoracic Doppler echocardiography. Patients were assessed preoperatively and before discharge from the hospital. A total of 20 patients received a stentless (homograft or Toronto) valve, and 13, a stented valve. No patient had significant aortic regurgitation or other valvular disease. Preoperatively, fractional shortening was 18.8+/-5.5% in the stentless group and 18.6+/-3.8% in the stented group. Postoperatively, it was 25.6+/-6.9% (P<0.001 compared with baseline) and 17.0+/-2.8%, respectively (P<0.001 compared with stentless group). Fractional shortening improved because of a reduction in LV end-systolic and end-diastolic dimensions in the stentless group. Systolic long axis function at the LV free wall also recovered, with an increase in systolic excursion and both peak shortening and lengthening rates. No change was noted in mitral valve Doppler patterns. CONCLUSIONS: Patients who received a stentless valve demonstrated a significantly greater early improvement in LV systolic function compared with those who received a stented valve.

Aged↗
PubMed1999

Pulmonary autograft versus aortic homograft for rereplacement of the aortic valve: results from a subset of a prospective randomized trial.

BACKGROUND: The use of a pulmonary autograft for rereplacement of the aortic valve has both potential advantages and disadvantages. This study details the early results of a subset of patients enrolled in a prospective randomized trial comparing pulmonary autografts and aortic homografts who have had previous aortic valve replacements. METHODS AND RESULTS: A total of 47 patients who had undergone >/=1 previous aortic valve replacement were randomized to receive either a pulmonary autograft (24 patients aged 40+/-11 years) or an aortic homograft (23 patients aged 37+/-11 years) for rereplacement of the aortic valve. One early death occurred in the homograft group, and 1 late (7 months) death occurred in the autograft group. One patient who received a pulmonary autograft was reoperated on for inflammatory pulmonary stenosis. One patient in each group was reopened for bleeding (both within 24 hours). Two patients in the autograft group had postoperative neurological weakness; they fully recovered over 2 months. Hospital stay, blood loss, incidence of perioperative arrhythmia, and markers of coronary ischemia were similar between the 2 groups. At 6-month follow-up (range, 1 to 12 months), left ventricular end-diastolic diameter was similar in both groups (homografts, 5.0+/-0.9 cm; autografts, 5.2+/-0.6 cm; P=NS), and no patient in either group had significant aortic valve dysfunction. CONCLUSIONS: Rereplacement of the aortic valve with a pulmonary autograft is feasible and safe in patients aged 14 to 60, regardless of their preoperative diagnosis or clinical condition.

Adolescent↗
PubMed1999

Right ventricular function after pulmonary autograft replacement of the aortic valve.

BACKGROUND: The pulmonary autograft operation (the Ross procedure) involves excision of a portion of the right ventricular (RV) outflow tract, prolonged cross-clamp times, and insertion of a pulmonary homograft. There is concern about the effect of such operations on right ventricular function. METHODS AND RESULTS: Twenty-five patients undergoing either pulmonary autograft or homograft replacement of the aortic valve as part of a prospective randomized trial had echocardiographic RV long-axis measurements performed before surgery and 6 months (range 3 to 12 months) after surgery. In all patients, systolic excursion (SE) and both shortening and lengthening rates (SR and LR, respectively) were reduced postoperatively (P<0.05) (homografts: SE 1.5+/-0.4 versus 2.3+/-0.6 cm, SR 6.8+/-2.1 versus 9. 6+/-3.1 cm/s, LR 6.0+/-1.8 versus 8.9+/-3.0 cm/s; autografts: SE 1. 4+/-0.4 versus 2.2+/-0.4 cm, SR 5.8+/-3.0 versus 8.2+/-3.0 cm/s, LR 5.7+/-1.9 versus 8.5+/-3.7 cm/s). There were no differences between the 2 groups. Eighteen patients who had undergone either aortic homograft or pulmonary autograft surgery were studied between 6 and 35 months after surgery. RV volumes were assessed with the use of MRI in addition to echocardiographic RV long-axis measurements. Global volumes were increased to a similar amount in both groups (homografts: end-diastolic volume 145+/-34 mL, end-systolic volume 78+/-23 mL; autografts: end-diastolic volume 157+/-33 mL, end-systolic volume 89+/-25 mL; P=NS), whereas stroke volumes were maintained in both groups (homografts 67+/-15 mL, autografts 67+/-16 mL; P=NS). RV SE was depressed in both groups to a similar degree to that seen with the previous group (homografts 1.5+/-0.3 cm, autografts 1.4+/-0.2 cm). CONCLUSIONS: Aortic valve replacement with either a pulmonary autograft or an aortic homograft leads to a degree of persistent RV longitudinal dysfunction that is not more pronounced in those undergoing the Ross procedure. The mechanisms and long-term effects of these changes must be further studied.

Adolescent↗
PubMed1999

Myocardial dysfunction in donor hearts. A possible etiology.

BACKGROUND: Potential cardiac donors show various degrees of myocardial dysfunction, and the most severely affected hearts are unsuitable for transplantation. The cause of this acute heart failure is poorly understood. We investigated whether alterations in calcium-handling proteins, beta-adrenoceptor density, or the inhibitory G protein Gialpha could account for this phenomenon in unused donor hearts (n=4 to 8). We compared these with end-stage failing hearts (n=14 to 16) and nonfailing hearts (n=3 to 12). METHODS AND RESULTS: Myocardial samples were obtained from unused donor hearts displaying ejection fractions <30%. Both trabeculae and isolated myocytes responded as poorly as those from the group of failing hearts to increasing stimulation frequency with regard to inotropic function in vitro. Immunodetectable abundance of sarcoplasmic reticulum calcium-ATPase and sodium calcium exchanger were greater (177%; P<0.01) and smaller (29%; P<0.01), respectively, in the unused donor hearts relative to the failing group, which suggests that alterations of these proteins are not a common cause of contractile dysfunction in the 2 groups. Myocytes from the unused donor group were desensitized to isoprenaline to a similar degree as those from the failing heart group. However, beta-adrenoceptor density was reduced in the failing (P<0.001) but not in the unused donor heart group (P=0.37) relative to the nonfailing heart group (n=5). Gialpha activity was increased in samples from unused donor and failing hearts relative to nonfailing hearts (P<0.05). CONCLUSIONS: Increased activity of the inhibitory G protein Gialpha is a significant contributory factor for impaired contractility in these acutely failing donor hearts.

Adolescent↗
PubMed1999

Early changes in the time course of myocardial contraction after correcting aortic regurgitation.

BACKGROUND: Correcting aortic regurgitation causes significant changes in left ventricular loading conditions, but few observations have been made intraoperatively of early effects on myocardial function. METHODS: We studied 18 patients (mean age, 59+/-12 years; 14 men) in whom aortic regurgitation was corrected with a stentless biologic valve. Overall left ventricular function was studied by thermodilution cardiac output, ventricular filling pressure, and systemic arterial pressure. Regional myocardial function was assessed from intraoperative transesophageal M-mode echocardiography and high fidelity ventricular pressure recordings before cardiopulmonary bypass, and 0.5, 1, 3, 6, 12, and 20 hours after operation. Time course of contraction, and magnitude of left ventricular systolic wall stress, dimensional shortening, myocardial power, and stroke work were measured. RESULTS: Global hemodynamics: there was an immediate decrease in left ventricular stroke volume (58+/-31 mL versus 80+/-30 mL, p = 0.004) and stroke work index (250+/-86 mJ/m versus 401+/-198 mJ/m, p = 0.005), but systemic arterial pressure (79+/-11 mm Hg versus 65+/-10 mm Hg, p = 0.002), increased at constant heart rate and end-diastolic pressure. Regional myocardial function and timing: peak systolic wall stress, dimensional shortening rate, and myocardial power production were all unchanged with operation. However, myocardial stroke work decreased (3.0+/-1.3 mJ/cm versus 4.8+/-2.4 mJ/cm, p = 0.009), attributable to shortening of the duration of systole (475+/-91 ms versus 543+/-67 ms, p<0.001). Diastolic time increased from 34%+/-18% to 71%+/-33% of systolic pulse duration (p<0.001). CONCLUSIONS: Correcting aortic regurgitation causes an early decrease in regional and global stroke work and increases diastolic time, although systolic wall stress does not decrease immediately. These beneficial effects are achieved by reducing the duration rather than altering the peak intensity (power) of myocardial contraction.

Adult↗
PubMed1999

The relationship of myocardial stroke work to coronary flow velocity immediately after aortic valve replacement.

BACKGROUND: The interrelations between myocardial stroke work and coronary flow velocity have not been fully defined during aortic valve replacement or with different cardioplegias. METHODS: Twenty-six patients (15 men age 63+/-13 years) who had elective isolated aortic valve replacement were studied by transesophageal Doppler echocardiography with simultaneous high fidelity left ventricular pressure. Fifteen patients received cold blood cardioplegia and 11 had warm blood cardioplegia. Myocardial stroke work and flow velocities in proximal left anterior descending coronary artery were quantified simultaneously before cardiopulmonary bypass and at 1, 6, 12, and 20 hours afterwards. RESULTS: Myocardial stroke work decreased postoperatively in both groups (160+/-19 versus 228+/-19 mJ/cm3 per minute, with cold blood cardioplegia; 135+/-22 versus 227+/-22 mJ/cm3 per minute with warm blood cardioplegia; both p<0.001 versus time, but p>0.05 versus cardioplegia, by two-way analysis of variance). Left anterior descending artery flow velocity-time integral per minute increased significantly in both groups (26.1+/-2.1 versus 15.0+/-2.1 m/min with cold blood cardioplegia; 32.8+/-2.5 versus 14.4+/-2.5 m/min with warm blood cardioplegia; both p<0.001 versus time, but p>0.05 versus cardioplegia). Thus, at 1 hour postoperatively the mJ x cm(-3) x m(-1) x min ratio of myocardial stroke work to left anterior descending artery flow velocity-time integral decreased significantly in both groups (4.3+/-1.6 versus 16.3+/-1.7 mJ x cm(-3) x m(-1) x min with warm blood cardioplegia, and 7.4+/-1.4 versus 17.9+/-1.4 J x cm(-3) x m(-1) x min with cold blood cardioplegia; both p<0.001 versus time). Warm blood cardioplegia was also associated with a lower mean ratio perioperatively than that with cold blood cardioplegia (7.8+/-0.9 versus 10.9+/-0.7 mJ x cm(-3) x m(-1) x min, p = 0.014). CONCLUSIONS: Coronary hyperemia occurs for at least 20 hours postoperatively when myocardial stoke work has decreased. The ratio of myocardial stroke work to coronary flow velocity appears to be more sensitive than either alone in differentiating the effect of warm versus cold blood cardioplegia.

Aortic Valve↗