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Biomedical subjects

J M Pinto

Publications and source records attributed to J M Pinto.

At least 19 recordsLinked to original sources

Efficient MILP formulations for the optimal synthesis of chromatographic protein purification processes.

The use of recombinant proteins has increased greatly in recent years, as well as the techniques used for their purification. The selection of an efficient process to purify proteins is a major bottleneck found when trying to scale up results obtained in the laboratory to a large-scale industrial process. One of the main challenges in the synthesis of downstream purification stages in biotechnological processes is the appropriate selection and sequencing of chromatographic steps. The objective of this work is to develop mixed integer linear programming models for the synthesis of protein purification processes. Models for each chromatographic technique rely on physicochemical data of a protein mixture, which contains the desired product and provide information on its potential purification. Formulations that are based on convex hull representations are proposed to calculate the minimum number of steps from a set of chromatographic techniques that must achieve a specified purity level and alternatively to maximize purity for a given number of steps. The proposed models are tested in several examples with experimental data and present time reductions of up to three orders of magnitude when compared to big-M formulations.

Biotechnology↗

Process performance models in the optimization of multiproduct protein production plants.

In this work we propose a model that simultaneously optimizes the process variables and the structure of a multiproduct batch plant for the production of recombinant proteins. The complete model includes process performance models for the unit stages and a posynomial representation for the multiproduct batch plant. Although the constant time and size factor models are the most commonly used to model multiproduct batch processes, process performance models describe these time and size factors as functions of the process variables selected for optimization. These process performance models are expressed as algebraic equations obtained from the analytical integration of simplified mass balances and kinetic expressions that describe each unit operation. They are kept as simple as possible while retaining the influence of the process variables selected to optimize the plant. The resulting mixed-integer nonlinear program simultaneously calculates the plant structure (parallel units in or out of phase, and allocation of intermediate storage tanks), the batch plant decision variables (equipment sizes, batch sizes, and operating times of semicontinuous items), and the process decision variables (e.g., final concentration at selected stages, volumetric ratio of phases in the liquid-liquid extraction). A noteworthy feature of the proposed approach is that the mathematical model for the plant is the same as that used in the constant factor model. The process performance models are handled as extra constraints. A plant consisting of eight stages operating in the single product campaign mode (one fermentation, two microfiltrations, two ultrafiltrations, one homogenization, one liquid-liquid extraction, and one chromatography) for producing four different recombinant proteins by the genetically engineered yeast Saccharomyces cerevisiae was modeled and optimized. Using this example, it is shown that the presence of additional degrees of freedom introduced by the process performance models, with respect to a fixed size and time factor model, represents an important development in improving plant design.

Automation↗

Lack of utility of postoperative chest radiograph in pediatric tracheotomy.

OBJECTIVE: To assess the incidence of pulmonary complications after nonemergent pediatric tracheotomy and to determine whether obtaining a routine postoperative chest radiograph is warranted. STUDY DESIGN: Retrospective review of the records of 107 consecutive patients (age 1 month to 18 years) who underwent tracheotomy from October 1994 to June 2000. Main outcome measures included frequency of pulmonary complications and use of information obtained from postoperative chest radiograph for intervention. SETTING: Tertiary care university children's hospital. RESULTS: No pneumothoraces or significant pulmonary complications were detected in the immediate postoperative period. No management changes were undertaken as a result of information obtained from any chest radiograph in this period. CONCLUSIONS: The incidence of significant pulmonary complications after pediatric tracheotomy is low. Little information is obtained from chest radiograph after tracheotomy, and this information does not change management. SIGNIFICANCE: Routine postoperative chest radiograph after pediatric tracheotomy is not indicated in all patients.

Adolescent↗

Systematic study of occult pulmonary thromboembolism in patients with deep venous thrombosis.

PURPOSE: This study was carried out to evaluate the prevalence and extension of pulmonary thromboembolism (PTE) in symptom-free patients with symptomatic deep venous thrombosis (DVT) of lower limbs and to evaluate their possible implication in the adequate treatment of thromboembolic disease. MATERIALS AND METHODS: We prospectively studied, using noninvasive examination (pulmonary spiral computed tomography [CT] angiography), 159 consecutive patients with acute DVT confirmed by duplex scanning without symptoms of PTE. CT was repeated at 30 days to study evolution of these clinically occult PTE. RESULTS: We observed silent PTE in 65 patients (41%) in all levels of lower limb venous thrombosis. Prevalence of PTE showed significant association with male sex (P =.001) and previously diagnosed heart disease (P =.023). There was no significant association between the level of DVT and the presence of PTE nor the DVT side and thromboembolic pulmonary localization. Of the 65 patients with positive CT exploration results for PTE, 52 had characteristics of acute PTE, 10 had chronic PTE, and 3 patients had both. Chronic PTE was found more frequently in patients with previous episodes of DVT (P =.024). A total of 165 pulmonary artery-affected segments were found at several locations: 5 main, 35 lobar, 58 interlobar, and 67 segmental. Multiple segments were affected in 59% of patients. Repeat CT examinations were performed at 30 days in 53 of 65 patients with positive CT scanning results. In 48 cases (90.6%) PTE had completely disappeared. CONCLUSIONS: Silent PTE occurred frequently in association with clots of lower limbs. The CT scan had a good availability and cost-effectiveness to detect clinically underestimated PTE. The incorporation of this exploration in the systematic diagnostic strategy of most patients with DVT to establish the extension of thromboembolic disease at diagnosis may be useful in the evaluation of added pulmonary artery symptoms and treatment strategies.

Adolescent↗

Electrical remodeling in ischemia and infarction.

This is a review of the electrophysiologic changes occurring at different times following myocardial infarction, both in the infarcted region (substrate) and in areas remote from the infarct. Regulators of channel function which might contribute to re-modeling, including autocrine/paracrine factors involved in ion channel gene regulation, are discussed.

Action Potentials↗

Characteristics of I(K) and its response to quinidine in experimental healed myocardial infarction.

INTRODUCTION: Mechanisms and drug treatment of serious ventricular arrhythmias in patients with healed myocardial infarction (HMI) are incompletely understood, in part because the electrophysiology and pharmacology of myocytes from noninfarcted regions of HMI hearts are not well characterized. METHODS AND RESULTS: We studied the delayed rectifier potassium current (I(K)) and quinidine responsiveness of single left ventricular subendocardial myocytes isolated from the region remote to the border zone of healed infarct myocardium (4 to 6 mm from scar edge) in cat hearts 2 months after coronary artery occlusion. Subendocardial cells isolated from corresponding regions of normal cat hearts provided controls. I(K) activation and tail currents were recorded using whole cell, voltage clamp techniques. Membrane capacitance of cells remote to HMI (187 +/- 7 pF) was significantly greater than normal (155 +/- 6 pF; P < 0.001). Action potential durations (APDs) recorded from myocytes in remote regions were prolonged (APD90 = 247 +/- 10 msec) compared to normal (214 +/- 11 msec; P < 0.05). Quinidine (1 microM) significantly prolonged APD90 in normal cells but not in remote cells. Density of I(K) (tail current) was significantly decreased in remote cells (3.1 +/- 0.3 pA/pF) compared to normal (3.9 +/- 0.3 pA/pF; P < 0.05), and voltage-dependent activation of I(K) was shifted in the positive direction. Quinidine had significantly less incremental blocking effect on I(K) already blunted by regional hypertrophy compared to its effect on normal cells in remote cells. IC50 shifted to 0.95 microM in remote cells compared with 0.50 microM in normal cells. CONCLUSION: Cells in noninfarct region remote from the scar are hypertrophied and display altered electrophysiology. Their reduced I(K) responsiveness to quinidine may explain, in part, failure of quinidine to prolong APD in such cells. Moreover, dispersion of repolarization may be decreased by the effect of quinidine on normal cells.

Action Potentials↗

Effects of mibefradil, a T-type calcium current antagonist, on electrophysiology of Purkinje fibers that survived in the infarcted canine heart.

INTRODUCTION: We studied the effects of mibefradil (MIB), a nondihydropyridine T-type Ca2+ channel antagonist, on T- and L-type Ca2+ (I(CaT), I(CaL)) currents in Purkinje myocytes dispersed from the subendocardium of the left ventricle of normal (NZPC) and 48-hour infarcted (IZPC) hearts. METHODS AND RESULTS: Currents were recorded with Cs+- and EGTA-rich pipettes and in Na+-K+-free external solutions to eliminate overlapping currents. In all cells, I(Ca) was reduced by MIB (0.1 to 10 microM). No change in the time course of decay of peak I(Ca) was noted. Average peak T/L ratio decreased in NZPCs but not IZPCs with 1 microM MIB. Steady-state availability of I(CaL) was altered with 1 microM MIB in both cell types (mean +/- SEM) (V0.5 = -22 +/- 4 mV for NZPC and -25 +/- 5 mV for IZPC before drug; -63 +/- 9 mV for NZPC and -67 +/- 6 mV for IZPC after drug; P < 0.05). For I(CaT), V0.5 (-50 +/- 3 mV for NZPC and -52 +/- 1 mV for IZPC before drug) shifted to -60 +/- 2 mV (NZPC) and -62 +/- 3 mV (IZPC) (P < 0.05) after drug. We also determined the effects of MIB on spontaneously beating Purkinje normal fibers and on depolarized abnormally automatic fibers from the infarcted heart using standard microelectrode techniques. When NZPC and IZPC fibers were superfused with [K+]o = 2.7 mM, MIB 3 microM and 10 microM had no effect on rate or the maximum diastolic potential, but action potential plateau shifted to more negative values, the slope of repolarization phase 3 decreased, and action potential duration increased. CONCLUSION: MIB blocks L- and T-type Ca2+ currents in Purkinje myocytes but lacks an effect on either normal or abnormal automaticity in Purkinje fibers.

Action Potentials↗

Reduced inward rectifying and increased E-4031-sensitive K+ current density in arrhythmogenic subendocardial purkinje myocytes from the infarcted heart.

INTRODUCTION: Subendocardial Purkinje myocytes from the 48-hour infarcted heart (IZPCs) have reduced resting potentials, possibly due to altered inwardly rectifying K+ currents IK1. Abnormal depolarization-activated outward K+ currents could contribute to long triangularly shaped action potentials of IZPCs. METHODS AND RESULTS: We used whole cell patch recordings to compare cesium-sensitive IK1 and 4-aminopyridine (4-AP)-resistant, noninactivating sustained IK between normal Purkinje myocytes (NZPCs) and IZPCs. IZPCs showed decreased net membrane currents. Two IZPC groups were distinguished, based on 4-AP-resistant outward K+ currents. IZPC-I had isochronal IK1 current-voltage relations similar to NZPCs whereas IZPC-II showed significantly reduced IK1 and increased outward plateau currents. To study the sustained IK in the presence of the Class III antiarrhythmic agent E-4031, a two-pulse protocol was used to inactivate transient outward currents, followed by step depolarizations. E-4031-sensitive currents were significantly greater in IZPCs at depolarized potentials (> 0 mV). Similar to NZPCs, IZPC E-4031 currents showed time dependence during depolarization, lack of rectification at positive steps, and voltage-dependent recovery from block. CONCLUSION: Decreased IK1 may account for reduced resting potentials in IZPCs. E-4031-sensitive currents in NZPCs, unlike those in canine ventricular myocytes, are sensitive to 4-AP and are larger in IZPCs.

4-Aminopyridine↗

Hypertrophy decreases cardiac KATP channel responsiveness to exogenous and locally generated (glycolytic) ATP.

This study tests the hypothesis that glycolytic regulation of KATP channel activity is altered in myocardial hypertrophy. Left ventricular (LV) subendocardial myocytes were isolated from cats with normal or left ventricular hypertrophied hearts (LVH). Saponin-permeabilized open cell-attached patch configurations of normal and LVH cells were exposed to an exogenous ATP consuming system containing hexokinase and 2-deoxyglucose. Phosphoenol pyruvate (PEP, substrate for the last ATP producing step in glycolysis) was applied extracellularly; ADP was present. In both cell types, KATP channels were activated in the absence of PEP, inhibited when PEP was added and activated again when PEP was removed, indicating the cells retained metabolic integrity and generated ATP in the proximity of their KATP channels. Single channel conductance in the absence of PEP was similar (70 pS, normal; 66 pS, LVH). However, LVH KATP channels showed enhanced activity (P0=0.50+/-0.03); normal (0.41+/-0.03) in PEP absence (P<0. 05). PEP responsiveness was reduced in LVH, with IC50, PEP increased to 23 microM; (11 microM normal). Lactate failed to activate KATP channels in both cell types. The concentration-P0 response curves obtained during exposure of open cells to exogenous ATP also revealed reduced responsiveness to ATP of LVH KATP channels (IC50, ATP=283 microM LVH; 93 microM normal). Our data indicate myocardial hypertrophy increases the maximal activity of KATP channels in the absence of ATP and reduces their responsiveness to ATP, including locally generated glycolytic ATP. These alterations in metabolic regulation of myocardial electrophysiology may contribute to diversity of action potential shortening in hypertrophied hearts during acute ischemia.

Adenosine Triphosphate↗

Plasma norepinephrine increased during coronary occlusion in hypertensive pigs that developed ventricular fibrillation.

Although hypertension is associated with increased risk of sudden cardiac death, the mechanisms involved remain enigmatic. Little is known about hemodynamic and plasma catecholamine concentration changes during coronary artery occlusion in hypertensive subjects. To study this, 30 pigs were implanted with catheters in the aorta and a silk snare around the left anterior descending coronary artery that could later be pulled to permanently occlude the artery. Perinephritic hypertension was induced in 14 of the animals over 3 weeks by wrapping one kidney in silk followed by contralateral nephrectomy. Coronary artery occlusion (CAO) was carried out in all pigs in the conscious resting state. Ventricular fibrillation (VF) developed in 50% of each group within 15 min after coronary artery occlusion. The hypertensive VF group showed an increase in norepinephrine concentration of 112 +/- 46%; a significantly greater increase than the intact VF group, which showed a 29 +/- 7% increase in norepinephrine concentration 5 min after coronary artery occlusion (p < 0.05).

Animals↗

Regional gradation of L-type calcium currents in the feline heart with a healed myocardial infarct.

INTRODUCTION: Abnormal action potentials in myocytes adjacent to > 2-month-old feline LV myocardial infarcts (MI) may reflect alterations in Ca2+ currents (Ica). METHODS AND RESULTS: We compared ICa, at 36 degrees C, in subendocardial myocytes isolated from areas adjacent to MI and to ICa in cells from remote areas (> 4 mm away; REM) and control cells from similar regions in normal hearts. Control (CON) myocytes had membrane capacitance of 234 +/- 10 pF (n = 81 cells) compared to 305 +/- 14 pF in REM (71 cells; P < 0.05 from CON) and 237 +/- 11 pF (n = 55 cells) in MI (not different from CON). From Vh = -40 mV; peak ICa elicited by test potentials (-35 to +70 mV) were significantly larger in CON (-1746 +/- 123 pA) and REM (-1795 +/- 142 pA) compared to MI (-1352 +/- 129 pA) (P < 0.05). Peak ICa density was significantly reduced in REM (-6.0 +/- 0.4 pA/pF) or MI (-5.7 +/- 0.4 pA/pF, P < 0.05) compared to CON (-7.5 +/- 0.4 pA/pF). Double exponential ICa decay was similar among groups. Half-inactivation potential (V0.5) was significantly shifted (hyperpolarizing direction) for MI (-29.1 +/- 2.6 mV) and REM (-24.6 +/- 1.2 mV) myocytes compared to -20.3 +/- 1.0 mV in CON. MI slope factor (k; 9.0 +/- 0.5) was significantly different from CON (6.8 +/- 0.3) and REM (7.3 +/- 0.4). No differences in time course of recovery from inactivation were noted. Five millimolar Ba2+o produced significant increases in ICa in CON and REM but an attenuated response in MI. Bay K8644 (1 microM) produced similar ICa increase in all groups. ICa increase due to isoproterenol (1 microM) in MI and REM was half that in CON, but there were no differences in increased ICa responses among groups following phenylephrine (10 microM). CONCLUSION: Reduced ICa density in REM reflects cell hypertrophy, whereas altered ICa of MI may reflect altered channel structure and/or function.

Action Potentials↗

Effects of beta adrenergic receptor blockade on hemodynamic changes associated with obstructive sleep apnea.

To study the effects of airway obstruction (AWO) and arousal on coronary blood flow, mean arterial pressure (MAP) and heart rate (HR), pigs were chronically instrumented with arterial catheters, Doppler flow probes on the left circumflex coronary artery, and electrodes for determination of sleep stages. A modified balloon catheter was placed in the trachea to obstruct the upper airway during sleep. Following control studies, the role of beta adrenergic receptors in hemodynamic responses to AWO was assessed by administering propranolol, a beta adrenoreceptor blocking agent. In control studies, during nonrapid eye movement sleep (NREM), MAP was 85 +/- 2 mmHg before AWO and increased by 8 +/- 2 mmHg upon arousal. Mean arterial pressure was lower during rapid eye movement (REM) sleep (64 +/- 2 mmHg) and the increase upon arousal was threefold greater (22 +/- 2 mmHg). Heart rate was similar in both sleep stages (NREM 123 +/- 5 bpm; REM 125 +/- 6 bpm) and increased significantly upon arousal (NREM, 11 +/- 2 bpm; REM, 18 +/- 3 bpm increase). Coronary blood flow was similar during both stages (NREM 44 +/- 5 ml/min; REM 44 +/- 6 ml/min) and increased by 13% (NREM) and 22% (REM) during arousal. Coronary vascular resistance increased significantly by 17% during arousal from AWO during REM sleep. All changes were significant at p < 0.05. Following beta adrenergic receptor blockade studies using propranolol, baseline HR was reduced in NREM sleep and HR and coronary blood flow increases during arousal from apnea were eliminated. Adrenoreceptor blockade studies suggest that these effects were mediated by the beta adrenergic component of the sympathetic nervous system.

Adrenergic beta-Antagonists↗

Reduced calcium currents in subendocardial Purkinje myocytes that survive in the 24- and 48-hour infarcted heart.

BACKGROUND: The abnormal transmembrane action potentials of subendocardial Purkinje fibers that survive 24 to 48 hours after coronary artery occlusion can be a source of the multiform ventricular tachycardias that occur during this time. A change in the density or function of either or both the T-type and L-type cardiac Ca2+ channels may contribute to the altered electrical activity of these Purkinje myocytes. METHODS AND RESULTS: The purpose of this study was to determine the function of the T- and L-type Ca2+ currents (iCat and iCaL, respectively) in Purkinje myocytes dispersed from the subendocardium of the left ventricle 24 and 48 hours after coronary artery occlusion (IZPC24 and IZPC48, respectively). To do this we compared whole-cell Ca2+ currents from Purkinje myocytes enzymatically dispersed from free-running fiber bundles (SPCs), from the subendocardium of the noninfarcted canine heart (NZPCs), and from IZPC24 and IZPC48. ICaL and iCat were recorded with Cs(+)- and EGTA-rich pipettes and in Na(+)-K(+)-free external solutions to eliminate overlapping currents. ICaL density was significantly reduced in IZPC48 compared with NZPC or IZPC24. This was not accompanied by a shift in the current-voltage relation or by a change in the time course of decay of iCaL. Replacement of Ca2+ with equimolar Ba2+ increased iCaL density in all cell types, but peak iBaL of IZPC48 remained reduced compared with control iBaL values. T-type Ca2+ currents were recorded in all SPCs and NZPCs. In IZPC24 and IZPC48 there was a reduction in peak iCat amplitudes and densities. This was not accompanied by a shift in the current-voltage relation or by a change in the time course of decay of peak iCat. However, there was a hyperpolarizing shift in the steady-state availability relations in both IZPC24 and IZPC48. In addition, the maximally available iCat in IZPC24 was not different from control, whereas it was significantly reduced in IZPC48. CONCLUSIONS: The L-type ICa density in subendocardial Purkinje myocytes that survive in the infarcted heart is significantly decreased by 48 hours after the time of coronary artery occlusion. The peak T-type ICa density is decreased in subendocardial Purkinje myocytes that survive in the infarcted heart at 24 hours, but further reduction occurs in these myocytes by 48 hours. This loss in Ca2+ channel function could contribute to the abnormal transmembrane potentials of these myocytes surviving in the infarcted heart.

Animals↗

Plasma norepinephrine changes after arousal and exercise were enhanced in conscious pigs with perinephritic hypertension.

This study found that pigs in the early stages of perinephritic hypertension had enhanced plasma norepinephrine (NE) and heart rate (HR) responses to behaviorally arousing stimuli (lifting in a canvas sling) and exercise. In the hypertensive animals, the increase in plasma NE in response to behavioral arousal caused by lifting was double that of the intact group, and the HR response was 50% greater. The increase in plasma NE in response to exercise was six times greater in hypertensive pigs. By contrast, mean arterial pressure changes were not enhanced in the hypertensive group. Exaggerated catecholamine responses in plasma to lifting and exercise stimulation were present when hemodynamic responses were not exaggerated.

Animals↗

Endocardial mapping of reentry around an anatomical barrier in the canine right atrium: observations during the action of the Class IC agent, flecainide.

INTRODUCTION: Flecainide is effective in terminating stable atrial flutter in the conscious dog with a Y-shaped right atrial lesion. In this model, flutter is due to circus movement of the impulse around a fixed anatomical barrier. METHODS AND RESULTS: To investigate the mechanism of flecainide-induced termination of this type of reentry, we determined the pattern of endocardial activation of the right and left atria before and during administration of flecainide by recording simultaneously from 192 electrode pairs in the isolated blood perfused heart. At least five consecutive flutter beats were analyzed before and during flecainide for each of eight termination episodes in five hearts. In all, flecainide increased flutter cycle length (164 +/- 24 msec) by 89% to 309 +/- 77 msec (P < 0.05) before termination. Atrial refractory period and conduction time during paced beats were also increased by flecainide. In five episodes, termination was due to conduction block of the impulse at critical sites within the reentrant circuit (mode 1). Cycle length oscillations (+/- 30 msec) at sites proximal to site of block preceded termination in three of these episodes. In three other episodes, interruption of the original circuit occurred when there was failure of a lateral boundary, giving rise to an impulse that reset the original circuit (mode 2). In these episodes, long-short cycle length oscillations led to return reexcitation by the impulse within the primary path and subsequent termination. CONCLUSION: In summary, similar to our previous findings with the Class III agent, d-sotalol, two different modes of termination of atrial reentry were observed with flecainide.

Animals↗

Hemodynamic changes associated with obstructive sleep apnea followed by arousal in a porcine model.

To study the effects of airway obstruction (AWO) and arousal on coronary blood flow, mean arterial pressure (MAP), and heart rate, pigs were chronically instrumented with arterial catheters, Doppler flow probes on the left circumflex coronary artery, and electrodes for determination of sleep stages. A modified tracheostomy tube was placed in the trachea to obstruct the upper airway during sleep sessions. In control studies, during non-rapid-eye-movement (NREM) sleep, MAP was 84 +/- 2 mmHg before AWO and increased by 5 +/- 2 mmHg on arousal. MAP was lower during rapid-eye-movement (REM) sleep (62 +/- 2 mmHg), and the increase on arousal was fourfold greater (22 +/- 2 mmHg). Heart rate was similar in both sleep stages (NREM: 120 +/- 4 beats/min; REM: 124 +/- 5 beats/min) and increased significantly on arousal (NREM: 12 +/- 2 beats/min; REM: 18 +/- 1 beats/min). Coronary blood flow was similar during both stages (NREM: 43 +/- 4 ml/min; REM: 46 +/- 8 ml/min) and increased by 12-15% on arousal. Coronary vascular resistance index increased significantly by 24% on arousal from AWO during REM sleep. All increases and decreases were significant at P < 0.05. Receptor blockade studies were performed to assess alpha-adrenergic receptor involvement.

Airway Obstruction↗

Transient coronary stenosis associated with arrhythmia and ischemia 24 hours after reperfusion.

We examined the electrophysiologic sequelae of transient reductions in coronary blood flow (CBF) in conscious dogs. Animals were instrumented to measure arterial pressure, heart rate, repetitive extrasystole threshold (RET), and CBF before coronary stenosis, during 90 minutes of a 50% reduction in CBF, and at 1, 24, 48, and 72 hours after reperfusion. RET was decreased at 24 and 48 hours but returned to baseline by 72 hours after reperfusion. Frequent ventricular ectopic activity (VEA), absent during the control period, was noted during stenosis and at 1, 24, and 48 hours after reperfusion. beta-Adrenergic blockade (metoprolol) normalized the decreased RET at 24 hours. Addition of alpha 1-adrenergic blockade (prazosin) abolished VEA. Endocardial blood flow in the posterior papillary muscle of the left ventricle was reduced by 52 +/- 9% during stenosis, was similar to baseline levels by 1 hour after reperfusion, and decreased by 39 +/- 5% at 24 hours. We conclude that episodes of modest coronary artery stenosis may be followed by electrophysiologic changes indicative of increased vulnerability to malignant ventricular arrhythmias.

Animals↗