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Biomedical subjects

R J Applegate

Publications and source records attributed to R J Applegate.

At least 37 records · Page 2Linked to original sources
PubMed1992

Indications, types, results, and complications of valvular surgery.

Results of long-term follow-up of new mechanical valves introduced in the 1980s and innovative new surgical techniques complementing repair of the mitral apparatus are discussed here. In addition, recent reports highlighting new information about the indications, types, results, and applications of valve surgery are described.

Bioprosthesis↗
PubMed1992

Restraining effect of intact pericardium during acute volume loading.

To determine the effect of the intact pericardium on ventricular end-diastolic pressures (EDP) during acute volume loading, we measured left ventricular (LV) and right ventricular (RV) micromanometer pressure and LV volume using a conductance catheter in eight open-chest, anesthetized dogs. A range of LV pressure and volume was obtained by intravascular volume expansion with the pericardium intact and then over a similar range after removal of the pericardium. Pericardial pressure (Pper) was calculated using static equilibrium analysis as the difference between LVEDP with the pericardium present and absent at a constant LV volume. At the beginning of the fluid infusion (LVEDP 7.3 +/- 1.7 mmHg and RVEDP 4.4 +/- 2.6 mmHg, mean +/- SD), Pper was not different from zero (-1.0 +/- 2.3 mmHg, P not significant). The onset of pericardial restraint (Pper greater than or equal to 0 mmHg) occurred when LVEDP was 9.1 +/- 2.9 mmHg and RVEDP was 4.1 +/- 2.9 mmHg. At low cardiac volumes before fluid infusion, RV transmural pressure was positive and significantly greater than the near zero Pper. After the onset of pericardial restraint, however, RVEDP and Pper increased similarly and were related according to Pper = 1.1 (+/- 0.34) RVEDP - 4.2 (+/- 2.6) mmHg, standard deviation 0.6 +/- 0.8 mmHg, r = 0.98 +/- 0.10. These data indicate that the intact pericardium behaves in two functionally distinct ways. At low cardiac volumes, Pper is zero and the pericardium does not affect LV filling. RV transmural pressure is positive and greater than Pper.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

The underlying coronary lesion in myocardial infarction: implications for coronary angiography.

Myocardial infarction is usually caused by sudden thrombotic occlusion of a coronary artery at the site of a fissured atherosclerotic plaque. Recent evidence suggests that coronary angiography may be insensitive in detecting and quantitating atherosclerosis. Serial angiographic studies demonstrate that the majority of myocardial infarctions occur due to occlusion of arteries that previously did not contain angiographically significant (greater than 50%) stenoses. Similarly, quantitative angiography performed after thrombolytic therapy indicates that the coronary lesion underlying the clot is frequently not severely stenotic. Thus, an angiographically apparent stenosis is not necessary for the development of a thrombotic occlusion resulting in an MI. These observations suggest that coronary angiography does not accurately predict the site of a subsequent occlusion that will produce a myocardial infarction.

Autopsy↗
PubMed1991

Load dependence of left ventricular diastolic pressure-volume relations during short-term coronary artery occlusion.

We evaluated the effect of altered loading conditions on left ventricular (LV) diastolic pressure-volume relations during acute coronary artery occlusion that was produced by inflation of an intracoronary balloon. Open-chest anesthetized dogs (n = 18) were instrumented so that LV pressure (micromanometer) and LV volume (conductance) could be measured without disturbing the pericardium. The effects of brief periods of occlusion (1-2 minutes) were assessed under steady-state conditions before and after dextran infusion with the pericardium present and absent and during vena caval occlusion. Under steady-state conditions before dextran infusion with the pericardium removed, at an LV end-diastolic pressure (EDP) of 8.4 +/- 1.4 mm Hg, occlusion resulted in a rightward shift in the diastolic portion of the LV pressure-volume loop (delta LVEDP, 2.7 +/- 2.3 mm Hg; delta LVEDV, 6.3 +/- 4.7 ml, both p less than 0.05 versus control). After dextran infusion (LVEDP, 20.9 +/- 6.0 mm Hg), occlusion resulted in a rightward and upward shift in the diastolic portion of the LV pressure-volume loop (delta LVEDP, 5.8 +/- 4.4 mm Hg; delta LVEDV, 4.2 +/- 3.0 ml, both p less than 0.05 versus control). At low cardiac volumes before dextran infusion, the intact pericardium did not affect the response to occlusion. By contrast, after dextran infusion in the presence of an intact pericardium, LVEDP significantly increased (delta, 6.4 +/- 3.6 mm Hg, p less than 0.05) but LVDEV did not (delta, 0.7 +/- 1.5 ml, p = NS). There was a parallel upward shift in the diastolic portion of the LV pressure-volume loop that was eliminated by removal of the pericardium. Thus, the change in LV diastolic pressure and volume during occlusion varied and depended on the baseline cardiac volume and presence of the pericardium. Before dextran infusion with the pericardium present and absent, coronary artery occlusion did not alter the LV diastolic chamber stiffness parameter, which was calculated from the diastolic interval of an averaged steady-state beat (0.040 +/- 0.019 versus 0.036 +/- 0.015 mm Hg/ml, p = NS). After dextran infusion with the pericardium present and absent, coronary artery occlusion increased the LV diastolic chamber stiffness parameter (0.057 +/- 0.034 and 0.074 +/- 0.034 mm Hg/ml, both p less than 0.05 versus controls, respectively). Vena caval occlusion eliminated the shifts in the diastolic portion of the LV pressure-volume loop with the pericardium present and absent.(ABSTRACT TRUNCATED AT 400 WORDS)

Angioplasty, Balloon, Coronary↗
PubMed1990

External pressure of undisturbed left ventricle.

We evaluated the contribution of the thorax and the undisturbed pericardium to the external pressure of the euvolemic left ventricle in thirteen anesthetized dogs. Left ventricular (LV) end-diastolic pressure (EDP) in the euvolemic state was 7 +/- 2 mmHg initially and increased to 10 +/- 2 mmHg after the chest and pericardium were opened. LV end-diastolic volume (conductance catheter) was 43 +/- 20 ml initially and did not change after the chest or the pericardium was opened. Intrathoracic (PIT) and pericardial (PPER) pressures were calculated as the difference in LV chamber pressure before and after opening these spaces. Thus for the LV, PIT was -3 +/- 1 mmHg, and PPER was 0 +/- 2 mmHg. Isovolumic relaxation, early diastolic filling, and total diastolic filling were not significantly altered after the chest or pericardium was opened. Thus under euvolemic conditions in this model pericardial pressure is negligible, and the external pressure of the undisturbed left ventricle is negative and equal to intrathoracic pressure.

Animals↗
PubMed1990

Simultaneous conductance catheter and dimension assessment of left ventricle volume in the intact animal.

We compared left ventricle (LV) volume (V) simultaneously measured using the conductance catheter (VM) with volume calculated from three LV dimensions (VD) determined ultrasonically from endocardial crystals. Seven adult mongrel dogs (20-30 kg) were anesthetized and instrumented to measure micromanometer LV pressure and V. Three pairs of crystals were placed orthogonally in subendocardial positions and a conductance catheter was placed in the LV retrograde across the aortic valve. Under steady-state conditions, over the range of a single cardiac cycle, the relation between VM and VD was well described by a straight line. There was an excellent correlation of conductance and dimension volumes with r equal to 0.97 +/- 0.04 and SEE 0.8 +/- 0.5 ml. The gain (1/alpha) and parallel conductance volume (alpha VC) were constant. At lower volumes obtained during bicaval occlusion, however, the relation between VM and VD was curvilinear. 1/alpha and alpha VC both decreased as LVV fell. Thus, determination of absolute volume using the conductance catheter depended on the conditions under which the data were obtained. Under steady-state conditions, alpha VC calculated by both the saline method (mean +/- SD, 50 +/- 15 ml) and by regression of VM and VD, (45 +/- 21 ml) were similar. Consequently, absolute LV end-diastolic volumes and end-systolic volumes by the conductance and dimension methods were similar (53 +/- 14 ml and 38 +/- 14 ml vs. 56 +/- 17 ml and 44 +/- 16 ml, respectively, p = NS). When volume decreased during bicaval occlusion, there was a progressively greater decrease in VM as compared with VD. The absolute slope (EES) of the end-systolic pressure-volume relation (ESPVR) was consistently higher by the dimension method, group average, 16.3 +/- 7.6, than by the catheter, 8.5 +/- 5.9, p less than 0.05. The direction and magnitude of the change in EES at different inotropic states (autonomic blockade; dobutamine), however, was similarly measured by both the conductance catheter and dimension method. We conclude that the gain and offset of the conductance catheter are relatively constant at steady state but vary when volume is reduced by caval occlusion. Thus, the conductance catheter accurately measures absolute volumes at steady state but can underestimate the slope and position of the ESPVR when it is determined by caval occlusion. The conductance catheter does, however, accurately measure the directions and magnitude of change in contractile state.

Animals↗
PubMed1990

Comparative effects of pacing-induced and flow-limited ischemia on left ventricular function.

We compared left ventricular (LV) myocardial blood flow and function accompanying severe demand ischemia (rapid atrial pacing in the presence of critical bilateral coronary stenoses) and supply ischemia (complete bilateral coronary occlusion) of the same ischemic regions in 14 pentobarbital-anesthetized dogs. Pacing-induced ischemia resulted in pronounced reductions in average regional epicardial blood flow (0.8 +/- 0.4 vs. control 1.2 +/- 0.4 [+/- SD] ml/g/min, p less than 0.05) and endocardial blood flow (0.4 +/- 0.1 vs. control 1.3 +/- 0.3 ml/g/min, p less than 0.05). More severe reductions in average regional epicardial and endocardial blood flow were seen after bilateral coronary occlusion (BCO) (0.3 +/- 0.3 and 0.1 +/- 0.1 vs. control 1.3 +/- 0.3 ml/g/min, p less than 0.05, respectively). Hemodynamics of postpacing ischemia (PPi) were consistently characterized by systolic impairment including depressed systolic contractile performance [(+)dP/dtmax 1,281 +/- 442 vs. control 2,173 +/- 775 mm Hg/sec, p less than 0.05], ventricular dilation (left ventricular [LV] end-diastolic dimension [EDD] 47.6 +/- 7.8 vs. control 44.7 +/- 8.6 mm, p less than 0.05), and an increase in LV end-diastolic pressure (EDP) (14.4 +/- 2.8 vs. control 4.2 +/- 2.8 mm Hg, p less than 0.05). Abnormalities in early and late diastolic function with PPi included increased time constant of isovolumic relaxation (78.0 +/- 40.4 vs. control 46.4 +/- 20.5 msec, p less than 0.05) and increased chamber stiffness (1.9 +/- 0.77 vs. control 0.81 +/- 0.55 mm Hg/mm, p less than 0.05), respectively. The LV diastolic pressure-dimension relation, however, shifted upward and to the right in eight of nine animals, whereas an upward shift was observed in only one animal. Thus, in this model of postpacing ischemia, we observed contractile failure and passive changes in diastolic function. Alterations in ventricular function occurred consistently earlier and to a greater extent during BCO than PPi, including higher LVEDP (25.3 +/- 8.1 vs. 14.9 +/- 6.6 mm Hg, p less than 0.05), greater ventricular dilation (delta LVEDD 4.9 +/- 2.5 vs. 3.5 +/- 2.8 mm, p less than 0.05), and reduced minor-axis dimension shortening (3.3 +/- 3.1% vs. 6.5 +/- 3.6%, p less than 0.05). To detect potential qualitative differences in ventricular function between the two types of ischemia, we evaluated hemodynamics at comparable loading conditions (30 seconds to 1 minute of BCO).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Invasive evaluation of left ventricular diastolic performance.

Diastole can be divided into four phases: 1. isovolumic relaxation; 2. early filling; 3. diastasis; and 4. atrial systole. The amount of left ventricular (LV) filling that occurs during each of these phases depends on: 1. myocardial relaxation; 2. the passive characteristics of the LV; 3. the characteristics of the left atrium, pulmonary veins and mitral valve; and 4. the heart rate. When diastolic function is normal, the net effect of these factors results in LV filling sufficient to produce an adequate cardiac output, while mean pulmonary venous pressure is maintained below 12 mm Hg. Diastolic dysfunction is normally manifest as pulmonary congestion. In the absence of systolic dysfunction, abnormal diastolic performance is usually due to abnormal relaxation and/or changes in the passive LV characteristics, external compression or disease of the mitral valve and left atrium. Invasive studies can quantify the rate of myocardial relaxation from the time course of the fall of LV pressure during isovolumic relaxation and the passive LV properties from the LV diastolic pressure-volume relation. In addition, frame-by-frame analysis of contrast ventriculography and conductance determination of LV volume can quantify the pattern of LV diastolic filling. Normally, at rest, most LV filling occurs early in diastole. Conditions that produce diastolic dysfunction, such as LV hypertrophy and ischemia, are associated with reduced early diastolic filling and an augmented importance of atrial systole. It is important to recognize that such patterns can occur in patients without clinically apparent diastolic dysfunction and in normals if left atrial pressure is sufficiently elevated. Furthermore, a normal pattern can occur in patients with severe diastolic dysfunction. Reduced early diastolic filling in the absence of pulmonary congestion indicates the loss of diastolic reserve, since the left atrium is being used as a booster-pump. This pattern of diastolic filling in a patient with symptoms of pulmonary congestion suggests diastolic dysfunction, even if systolic LV performance is normal.

Atrial Function↗
PubMed1988

Acute total aortic occlusion during cardiac catheterization associated with polycythemia vera.

We present a case of acute total aortic occlusion at the time of cardiac catheterization in a 62-yr-old female with an acute myocardial infarction and newly diagnosed polycythemia vera. Despite normalization of serum viscosity and red cell mass by phlebotomy, her predisposition to thrombosis persisted. Caution is advised when considering cardiac catheterization in patients with this disease.

Acute Disease↗
PubMed1988

Osmotically released vasopressin augments cardiopulmonary reflex inhibition of the circulation.

Exogenous arginine vasopressin (AVP) has been shown to augment the inhibitory influence of arterial and cardiopulmonary baroreflexes. This study examined the influence of osmotically released AVP on the inhibitory responses to activation of cardiopulmonary receptors by administration of veratrum alkaloids. Three groups of conscious dogs, with carotid sinus intact, with prior sinoaortic denervation (SAD), and with prior lesion of the area postrema (AP), were instrumented for monitoring arterial pressure and heart rate and with left circumflex coronary artery or left atrial catheters for administration of veratrum alkaloids. Conscious dogs were administered veratridine (0.5-1.0 microgram.kg-1.min-1) under control conditions, after infusion of hypertonic saline (HS, 6% NaCl), and after HS in the presence of the AVP vascular (V1) receptor antagonist. In carotid sinus-intact dogs, veratridine reduced arterial pressure (-10 +/- 0.4 mmHg). After HS infusion, the depressor response to veratridine was significantly greater (-18 +/- 0.8 mmHg). The enhanced depressor response during HS infusion was prevented by administration of the AVP antagonist (-8 +/- 0.6 mmHg). Responses to veratrum alkaloids in SAD dogs were similar. In AP-lesioned animals, the depressor effects of veratridine (-9 +/- 0.5 mmHg) were similar to intact animals. However, the response to veratridine during HS was not altered (-9 +/- 0.8 mmHg) in AP-lesioned dogs. Results suggest that osmotically stimulated AVP augments the inhibitory effects of cardiopulmonary reflexes and that this effect is mediated through the area postrema via the V1 receptor.

Animals↗
PubMed1988

Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild-to-moderate coronary artery disease?

To help determine if coronary angiography can predict the site of a future coronary occlusion that will produce a myocardial infarction, the coronary angiograms of 42 consecutive patients who had undergone coronary angiography both before and up to a month after suffering an acute myocardial infarction were evaluated. Twenty-nine patients had a newly occluded coronary artery. Twenty-five of these 29 patients had at least one artery with a greater than 50% stenosis on the initial angiogram. However, in 19 of 29 (66%) patients, the artery that subsequently occluded had less than a 50% stenosis on the first angiogram, and in 28 of 29 (97%), the stenosis was less than 70%. In every patient, at least some irregularity of the coronary wall was present on the first angiogram at the site of the subsequent coronary obstruction. In only 10 of the 29 (34%) did the infarction occur due to occlusion of the artery that previously contained the most severe stenosis. Furthermore, no correlation existed between the severity of the initial coronary stenosis and the time from the first catheterization until the infarction (r2 = 0.0005, p = NS). These data suggest that assessment of the angiographic severity of coronary stenosis may be inadequate to accurately predict the time or location of a subsequent coronary occlusion that will produce a myocardial infarction.

Adult↗
PubMed1987

Usefulness of two-dimensional echocardiography during low-level exercise testing early after uncomplicated acute myocardial infarction.

To determine whether 2-dimensional (2-D) echocardiographic measures of segmental and global left ventricular (LV) function immediately on recovery of low-level, symptom-limited treadmill exercise are as sensitive as the same variables measured at peak bicycle exercise, 21 patients were studied after acute myocardial infarction (AMI). The recovery treadmill ejection fraction analysis was predictive of the peak bicycle results in 18 of the 21 patients (86%) and recovery treadmill wall motion abnormalities were predictive of the peak bicycle analysis in 17 (81%) (p less than 0.01). These data indicate that 2-D echocardiography during the immediate recovery phase of low-level postinfarction treadmill testing was as sensitive as the peak exercise assessment of segmental and global LV function. Accordingly, the predictive value of rest and recovery exercise measures were prospectively assessed in 67 patients during a mean follow-up interval of 11 months (range 3 to 24). Clinical characteristics and treadmill electrocardiographic findings did not identify the 16 of 67 patients (24%) who had new cardiac events (3 cardiac deaths, 8 recurrent AMIs and 6 coronary artery bypass graft operations). However, a decrease in recovery ejection fraction units of more than 10% was seen in 7 of these 16 patients (44%) with events, compared with only 4 of the 51 (13%) without events (p less than 0.002), and new or worsening wall motion abnormalities on exercise recovery were seen in 10 of the 16 patients (63%) with events, but in only 10 of the 51 (20%) without (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Vagal cold block in area postrema-lesioned dogs: interaction of vasopressin and sympathetic nervous system.

This study evaluated the interaction between arginine vasopressin (AVP) and the sympathetic nervous system (SNS) during bilateral vagal cold block (BVB) and the arterial baroreflex response to phenylephrine (PE) and exogenous AVP in conscious sham-operated (sham) and area postrema (AP)-lesioned mongrel dogs. The hemodynamic responses to ganglionic blockade (GB) and the vascular (V1) AVP receptor antagonist [d(CH2)5Tyr(Me)]AVP (AVPX) were similar in sham and AP-lesioned dogs. Elimination of the AVP pressor system by AVPX in sham dogs did not alter the pressor response to BVB, whereas subsequent blockade of the SNS by GB abolished the response to BVB. When GB was first imposed, however, it alone eliminated only 55% of the pressor response to BVB, whereas subsequent AVPX eliminated the remaining pressor response to BVB. In contrast, in AP-lesioned dogs, AVPX alone substantially reduced the pressor response to BVB. Additionally, the apparent contribution of each pressor system to the response to BVB was not enhanced in the absence of the other system, as had been seen in the sham dogs. These data indicate that during interruption of vagal afferent activity, reflexly released AVP appears to limit the reflex activation of the SNS. This interaction of AVP with the cardiopulmonary reflex is eliminated following ablation of the area postrema. Infusion studies with PE and AVP indicate that AVP significantly augments baroreflex inhibition of heart rate when compared with PE. Ablation of the area postrema did not alter the arterial pressure-heart rate relationship obtained with PE but eliminated the augmented response to AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗