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Biomedical subjects

J S Rankin

Publications and source records attributed to J S Rankin.

At least 19 recordsLinked to original sources
PubMed1997

Left ventricular adaptation to aortic regurgitation in conscious dogs.

OBJECTIVE: Cardiac failure as a result of valvular heart disease remains a major clinical problem that frequently leads to ventricular dysfunction, myocardial failure, and even death. The development of irreversible myocardial damage may be especially insidious in volume overload as a result of aortic or mitral regurgitation. METHODS AND RESULTS: Left ventricular wall volume, ventricular function, and myocardial performance were assessed in 10 chronically instrumented conscious dogs before and after creation of aortic regurgitation. Left ventricular wall volume was measured by serial echocardiography. Left ventricular function was assessed by total cardiac output, stroke work, the slope of the Frank-Starling relationship, and the slope of the end-systolic pressure-volume relationship. Myocardial performance was assessed by the slope of the myocardial power output versus end-diastolic strain relationship. End-diastolic wall stress and volume both increased acutely and remained elevated after creation of aortic regurgitation. Peak systolic wall stress increased initially (1 to 3 weeks) from 336 +/- 30 to 369 +/- 55 mm Hg but returned to control values as left ventricular wall volume increased from 78 +/- 13 to 88 +/- 16 ml after development of compensatory hypertrophy. Left ventricular systolic function remained constant or increased and was maintained initially by increased myocardial performance, which returned to baseline levels after the development of compensatory hypertrophy. CONCLUSIONS: Myocardial performance and ventricular function vary independently in aortic regurgitation. Measures of myocardial performance such as the myocardial power output versus end-diastolic strain relationship may be useful in clinical assessment of aortic regurgitation.

Animals↗
PubMed1996

Effects of valve replacement on ventricular mechanics in mitral regurgitation and aortic stenosis.

BACKGROUND: This study in humans assessed changes in left ventricular function early and late after correction of mitral regurgitation (MR) (n = 9) or aortic stenosis (AS) (n = 10). METHODS: Ventricular function was measured with radionuclide and micromanometer-derived pressure-volume loops during preload manipulation, thermodilution cardiac outputs, and echocardiograms. Late radionuclide and echocardiographic data were acquired at 24 hours and 20 months. RESULTS: Perioperative left ventricular performance (stroke work-end-diastolic volume relationship) did not change for patients with MR or AS. Significant changes in afterload occurred: ejection fraction (MR, 0.49 to 0.37; AS, 0.54 to 0.60; both, p = 0.013), mean left ventricular ejection pressure (MR, 73 to 91 mm Hg; AS, 138 to 93 mm Hg; both, p < 0.01), and end-systolic wall stress (MR, 26 to 42 x 10(3) dynes/cm2; AS, 37 to 22 x 10(3) dynes/cm2; both, p < 0.01). Ejection efficiency improved for MR patients (0.69 +/- 0.26 to 1.0 +/- 0.15; p < 0.05). The 20-month data showed improved New York Heart Association functional class, normal resting ejection fraction, and normal exercise response for both groups. CONCLUSIONS: Early after operation, a significant change in left ventricular load was seen with correction of MR and AS. Data obtained late after operation showed improvement consistent with ventricular remodeling.

Aged↗
PubMed1995

Origin of regional pressure gradients in the left ventricle during early diastole.

Left ventricular (LV) pressure (P)-diameter, LVP-area, or LVP-volume relationships used to evaluate LV diastolic function assume uniform LV wall motion and constant LVP. Contrary to these assumptions, there are significant differences in ventricular dynamic geometry and in LV pressures measured simultaneously in different parts of the LV, particularly during early diastole. We instrumented six anesthetized open-chest dogs with three pairs of orthogonal ultrasonic crystals (anterior-posterior and septal-free wall minor axes, and base-apex major axis) and two micromanometers (in the apex and in the LV base). The mitral valve occluder was implanted during standard cardiopulmonary bypass in the mitral annulus. Data were recorded during 11 transient vena caval occlusions. The mitral valve was occluded for 1 beat every 6-8 beats during each vena caval occlusion to produce nonfilling diastole. With the decrease of the LV end-systolic volume (Ves) below the equilibrium volume Veq (volume of the completely relaxed LV at LVP = 0); the minimum negative LVP in nonfilling beats increases, the shape of the ventricle is more ellipsoidal in both filling and nonfilling beats, and the base-to-apex pressure gradient at the time of LVP minimum increases regardless of the presence or absence of filling. Thus heterogeneous myocardial stresses during isovolumic relaxation and early diastole result in ventricular shape changes, intraventricular redistribution of chamber volume, local accelerations of blood, and associated intraventricular LVP gradients. The role of elastic recoil assumes greater importance at Ves smaller than Veq, when the left ventricle becomes more ellipsoidal in shape during isovolumic relaxation, leading, in turn, to greater shape changes and greater LVP gradient.

Animals↗
PubMed1994

Measurement of left ventricular volume in normal and volume-overloaded canine hearts.

Serial studies of adaptation to aortic regurgitation (AR) were undertaken to determine whether sonomicrometry and echocardiography could be combined to measure changes in left ventricular (LV) cavitary volume (Vlv) and wall mass using the geometric formula [Vlv = K pi b2 alpha--wall volume], where K is a constant depending on the geometric model and a and be are epicardial major- and minor-axis diameters, respectively. Postmortem studies were performed in six normal dogs and in nine with AR; ultrasonic ventricular dimensions were measured as Vlv was varied with an intracavitary balloon. Three models were tested: 1) ellipsoid (model I; K = 1/6), 2) cylinder-ellipsoid (model II; K = 5/24), and 3) cylinder (model III; K = 1/4). The slope of the relationship between calculated Vlv and balloon volume varied between models (I, 0.71 +/- 0.11; II, 0.89 +/- 0.14; III, 1.07 +/- 0.17), and empiric determination of K to produce a slope of 1.0 resulted in a value of 0.26 +/- 0.04, not significantly different from the cylindrical model. Serial measurements of LV dimensions in 10 chronically instrumented conscious dogs revealed no significant change in end-diastolic or end-ejection LV shape after up to 16 wk of AR. Sonomicrometry and echocardiography can be integrated using a cylindrical geometric model to accurately estimate changes in end-diastolic or end-ejection Vlv during chronic volume overload.

Animals↗
PubMed1994

Effects of cardiac glycosides on myocardial function and energetics in conscious dogs.

The physiological effects of intravenous ouabain on left ventricular (LV) systolic function and metabolic-to-mechanical energy transfer were examined in eight conscious dogs. LV pressure and volume were measured using micromanometers and ultrasonic dimension transducers during transient vena caval occlusions under control conditions and after increasing doses of ouabain. Doppler coronary flow and coronary sinus O2 saturations were used to determine arterial-to-coronary sinus O2 content difference and thereby to calculate LV O2 consumption; total mechanical energy was computed as the sum of LV stroke work and the product of end-diastolic volume and LV mean ejection pressure, neglecting LV unstressed cavitary volume. The slope (10(4) erg/ml) of the stroke work vs. end-diastolic volume relationship increased progressively with rising doses of ouabain from 7.0 +/- 1.6 at control to 9.6 +/- 1.7 after ouabain 0.75 mg (P = 0.0002). Regression analysis of LV O2 consumption (mW/cm3) vs. total mechanical energy (mW/cm3) yielded a linear relationship that did not change with 0.75 mg of ouabain (P > 0.4). These data indicate that ouabain possesses a significant positive inotropic effect on the intact left ventricle without a change in energy transfer efficiency or O2 wasting.

Animals↗
PubMed1994

Relationship of the proinflammatory cytokines to myocardial ischemia and dysfunction after uncomplicated coronary revascularization.

The proinflammatory cytokines have been implicated in mediating myocardial dysfunction associated with myocardial infarction, severe congestive heart failure, and sepsis. We tested the hypothesis that cytokine levels are elevated after uncomplicated coronary artery bypass grafting and associated with episodes of postoperative myocardial ischemia and dysfunction. Coronary artery bypass grafting was performed under general anesthesia with moderate systemic hypothermia and cold-blood potassium cardioplegic solution. Tumor necrosis factor-alpha and interleukin-6 levels were determined by bioassays, and interleukin-8 levels were measured by a sandwich enzyme-linked immunosorbent assay. Myocardial function and ischemic episodes were assessed by intraoperative transesophageal echocardiography and perioperative 12-channel Holter monitoring. A total of 22 patients were studied, with no deaths or complications. Arterial tumor necrosis factor-alpha rose in a bimodal distribution, peaking at 2 and 18 to 24 hours after the operation (at 20.2 +/- 6.4 pg/ml, [mean +/- standard error of the mean]) and 5.8 +/- 1.6 pg/ml, respectively; before cardiopulmonary bypass: 0.90 +/- 0.20 pg/ml, p < 0.001 for both peaks) then progressively declined to levels before bypass. Arterial interleukin-6 was maximally elevated immediately on termination of cardiopulmonary bypass and peaked again 12 to 18 hours after cardiopulmonary bypass (at 7520 +/- 2439 pg/ml and 6216 +/- 1928 pg/ml, respectively; before bypass: 746 +/- 187 pg/ml, p < 0.0001 for both peaks). Arterial interleukin-8 levels were more variable but followed a similar pattern, peaking in the early period after cardiopulmonary bypass and again at 16 to 18 hours after the operation (at 4110 +/- 1403 pg/ml and 1760 +/- 1145 pg/ml, respectively; before bypass: 461 +/- 158, p < 0.05 for both peaks). By multivariate analysis, the aortic crossclamp time was independently predictive of postoperative cytokine levels. Left ventricular wall motion abnormalities were associated with both interleukin-6 and interleukin-8 levels, worsening scores being associated with increasing levels (for interleukin-6, p = 0.003; for interleukin-8, p = 0.05). Postoperative myocardial ischemic episodes were associated with interleukin-6 levels, six of seven (85%) patients with episodes of myocardial ischemia after a peak in interleukin-6 concentrations (p < 0.01). We conclude that proinflammatory cytokines are elevated after uncomplicated coronary revascularization and may contribute to postoperative myocardial ischemia and segmental wall motion abnormalities.

Aged↗
PubMed1994

Influence of hyperbaric oxygen on left ventricular contractility, total coronary blood flow, and myocardial oxygen consumption in the conscious dog.

It is known that hyperbaric oxygenation (HBO) decreases total coronary blood flow (TCBF) and cardiac output (CO). To determine whether this is related to an alteration in myocardial contractility, 10 chronically instrumented conscious dogs were studied during pharmacologic autonomic blockade. Left ventricular (LV) volume was measured with ultrasonic transducers, LV transmural pressure with micromanometers, TCBF with Doppler-flow probes, and coronary AVO2 difference (A-CSO2) was calculated from direct LV and coronary sinus (CS) sampling. To evaluate the effect of increased oxygenation, data were obtained during resting control conditions and during dynamic vena caval occlusions (VCO), at 1 atmosphere of pressure, while breathing air (1 bar/0.21); at 3 atmospheres, breathing compressed air (3 bar/0.21), and at 3 atmospheres breathing 100% oxygen (3 bar/1.0). Because of autonomic blockade, heart rate (HR) was not statistically different in the three conditions. With increasing oxygenation, arterial oxygen tension (PaO2) increased from 85 +/- 5 mmHg (mean +/- SD) at 1 bar/0.21, to 1374 +/- 201 mmHg at 3 bar/1.0 whereas arterial carbon dioxide tension (PaCO2) and pH values were not statistically different. Arterial oxygen content (AO2 content) and CSO2 content increased significantly (both P < 0.05) with increasing PaO2. LV stroke volume (SV), CO, coronary blood flow, and myocardial oxygen consumption (MVO2) were all significantly reduced (P < 0.05) with increasing levels of oxygenation. Intrinsic myocardial function, as measured by the stroke-work/end-diastolic volume relationship was unchanged from 1 bar/0.21 to 3 bar/0.21, and to 3 bar/1.0 (P < 0.20). Thus, the diminished TCBF, CO, and MVO2 associated with HBO do not seem to be associated with a primary alteration in myocardial contractility, but rather may result from a physiologic autoregulation of the myocardium to increasing levels of PaO2.

Animals↗
PubMed1993

Balloon aortic valvuloplasty as a bridge to aortic valve replacement in critically ill patients.

This report highlights our experience in 5 patients with severe aortic stenosis and multiple organ failure undergoing balloon aortic valvuloplasty as a bridge to conventional aortic valve replacement. Balloon aortic valvuloplasty successfully stabilized the condition of these patients, improved organ function, and decreased their baseline risk profile. Elective aortic valve replacement was then performed without complications. Short-term palliation with balloon aortic valvuloplasty should be considered as a bridge to aortic valve replacement in selected patients with critical aortic stenosis and multiple organ failure.

Adult↗
PubMed1993

Use of Bachmann's bundle for bipolar atrial pacing.

In patients with acute or chronic right coronary ischemia, pacing with temporary right atrial epicardial wires is sometimes difficult due to high electrical thresholds. A simple and reproducible technique is described to assure atrial capture and appropriate atrial pacing under these conditions.

Cardiac Pacing, Artificial↗
PubMed1993

Comparison of balloon valvuloplasty with operative treatment for mitral stenosis.

To determine the optimal role for percutaneous balloon mitral valvuloplasty or open mitral commissurotomy, the outcome of 164 consecutive patients undergoing either percutaneous balloon mitral valvuloplasty, open mitral commissurotomy, or mitral valve replacement for mitral stenosis was reviewed. No preoperative differences existed between percutaneous balloon mitral valvuloplasty and open mitral commissurotomy in age, symptoms, or mitral valve characteristics. Symptoms improved similarly in all groups, and median hospital stays after procedures were 2, 9, and 10 days for percutaneous balloon mitral valvuloplasty, open mitral commissurotomy, and mitral valve replacement (p < 0.005). Actuarial survivals at 36 months did not differ significantly (83% +/- 6%, 94% +/- 4%, and 90% +/- 4%). Actuarial freedoms from subsequent mitral valve procedures at 36 months were 66% +/- 7%, 87% +/- 6%, and 100% +/- 13% (p < 0.005), with the linearized rate of subsequent mitral valve procedures being 12% +/- 3%, 4% +/- 2%, and 1.2% +/- 0.8%/patient-year for percutaneous balloon mitral valvuloplasty, open mitral commissurotomy, and mitral valve replacement (p < 0.01). Prior mitral commissurotomy increased the likelihood of subsequent mitral procedures after percutaneous balloon mitral valvuloplasty from 10% +/- 3% to 20% +/- 7%/patient-year.

Adult↗
PubMed1993

Recovery of myocardial function after repetitive episodes of reversible ischemia.

The question of whether recovery of regional myocardial function after repetitive, reversible ischemia differs from recovery after a single episode of myocardial ischemia remains controversial. Therefore, eight conscious dogs were instrumented with ultrasonic dimension transducers and left ventricular micromanometers. Each animal underwent (in random sequence, 72 h apart) a single 15-min left anterior descending coronary arterial (LAD) occlusion and two 15-min LAD occlusions separated by 1 h of reperfusion. The preload recruitable work area (PRWA; the area beneath the regional stroke work vs. end-diastolic length relationship) quantified regional myocardial performance. Repetitive ischemia significantly delayed recovery of PRWA over the first 24 h (P < 0.05). Although postischemic myocardial creep resolved rapidly after single occlusion, double occlusion prevented recovery of creep during the first 4 h of reperfusion. The recovery time course of PRWA paralleled the resolution of myocardial creep, suggesting that creep contributed significantly to delayed functional recovery and that myocardial "stunning" after repetitive ischemia may result in part from interaction between postischemic diastolic properties and systolic dysfunction.

Animals↗
PubMed1993

Physiology of cardiac tamponade and paradoxical pulse in conscious dogs.

The physiological mechanism of paradoxical pulse in cardiac tamponade remains controversial. In eight conscious dogs with intact pericardia, ultrasonic dimension transducers assessed biventricular geometry and volumes, while micromanometers measured right ventricular (RV), left ventricular (LV), pleural, and pericardial pressures. With normal inspiration, peak LV pressure fell by 7.7 +/- 1.3 mmHg at control and by 20.3 +/- 3.7 mmHg during tamponade (P < 0.001), consistent with the development of paradoxical pulse. At peak inspiration during tamponade, RV filling increased, the interventricular septum shifted leftward, transeptal pressure became negative, and LV septal arc length (l theta) became smaller than its respective unpreloaded value at maximal vena caval occlusion (l(o)). Analysis of stroke work (SW)-end-diastolic volume (EDV) and end-systolic pressure-volume coordinates at peak inspiration during tamponade revealed that end-systolic pressure was 19.1 +/- 10.2 mmHg below the baseline end-systolic pressure-volume curve (P < 0.01), and SW was 24.2 +/- 8.8% below the baseline SW-EDV curve (P < 0.01), indicating transient inspiratory LV dysfunction. It is proposed that inspiratory leftward interventricular septal shifting at low LV EDV during tamponade completely unloads the septum (l theta < l o), eliminates the septal contribution to global LV SW, results in transient inspiratory LV dysfunction, and contributes to the phenomenon of paradoxical pulse.

Animals↗
PubMed1993

Prognosis and management of anterolateral myocardial infarction in patients with severe left main disease and cardiogenic shock. The left main shock syndrome.

BACKGROUND: To identify the determinants of survival in patients with severe (> 75%) stenosis of the left main coronary artery (LM) and an acute (48 hours) anterolateral myocardial infarction (AAMI), we retrospectively analyzed the course of 34 such patients who presented to our institution over the last decade. METHODS AND RESULTS: LM disease was diagnosed arteriographically at presentation, and AAMI was determined by ECG, enzymatic, and kinetic criteria. Of the nine patients (26%) managed medically, seven patients (78%) were in cardiogenic shock (cardiac index < 2.0, left ventricular end-diastolic pressure > 25, and pulmonary edema), and all seven died in hospital. Twenty-five (74%) of the 34 patients were managed surgically or with angioplasty. Nine of these patients, of whom eight were in cardiogenic shock, also died in hospital. Regardless of the method of treatment, the presence of cardiogenic shock in this population was reproducibly a grave prognostic indicator. That is, 15 (94%) of the 16 patients in cardiogenic shock at presentation died in hospital, and only 1 (5%) of the 18 patients without cardiogenic shock died (P < .001). CONCLUSIONS: Thus, we propose that, because patients presenting with AAMI, severe LM stenosis, and cardiogenic shock (left main shock syndrome) have such a grave prognosis regardless of management, conservative measures may be indicated.

Aged↗
PubMed1992

Outcome of patients sustaining acute ischemic mitral regurgitation during myocardial infarction.

OBJECTIVE: To describe outcomes of patients sustaining an acute myocardial infarction complicated by mitral regurgitation managed with contemporary reperfusion therapies. DESIGN: Inception cohort case study. Long-term follow-up was obtained in 99% of all patients. SETTING: University referral center. PATIENTS: A series of 1,480 consecutive patients presenting between April 1986 and March 1989 who had emergency cardiac catheterization within 6 hours of infarction. Fifty patients were found to have moderately severe or severe mitral regurgitation. OUTCOME MEASURES: Mortality; follow-up cardiac catheterization in patients with regurgitation. RESULTS: Acute ischemic moderately severe to severe (3+ or 4+) mitral regurgitation was associated with a mortality of 24% at 30 days (95% CI, 12% to 36%), 42% at 6 months (CI, 28% to 56%), and 52% at 1 year (CI, 38% to 66%); multivariable analysis identified 3+ or 4+ mitral regurgitation as a possible independent predictor of mortality (P = 0.06). Patients with mitral regurgitation tended to be female, older, and to have cerebrovascular disease, diabetes, and preexisting symptomatic coronary artery disease. A physical examination did not identify 50% of patients with moderately severe to severe regurgitation. Acute reperfusion with thrombolysis or angioplasty did not reliably reverse valvular incompetence. In this observational study, the greatest in-hospital and 1-year mortalities were seen in patients reperfused with emergency balloon angioplasty, whereas patients managed medically or with coronary bypass surgery had lower mortalities. CONCLUSIONS: Moderately severe to severe (3+ or 4+) mitral regurgitation complicating acute myocardial infarction portends a grave prognosis. Acute reperfusion does not reduce mortality to levels experienced by patients with lesser degrees of mitral regurgitation nor does it reliably restore valvular competence.

Acute Disease↗
PubMed1992

Mechanical correlates of the third heart sound.

In seven chronically instrumented conscious dogs, micromanometers measured left ventricular pressure, and ultrasonic dimension transducers measured left ventricular minor-axis diameter; the latter recording was filtered to examine data between 20 and 100 Hz. Acceptable external heart sounds were recorded with a phonocardiographic microphone in four of the seven dogs. With each dog sedated, intubated and mechanically ventilated, data were obtained during hemodynamic alterations produced by volume loading, phenylephrine, calcium infusion and vena caval occlusion. Damped oscillations were noted consistently in the left ventricular diameter waveform toward the end of rapid ventricular filling. These wall vibrations, assessed by the filtered diameter, correlated well with the third heart sound (S3) on the phonocardiogram. The peak frequency of the wall vibrations increased with increased diastolic pressure (p = 0.004), probably reflecting an increase in myocardial wall stiffness. In contrast, the amplitude of the vibrations varied directly with left ventricular filling rate (p = 0.0001). Thus, S3 seemed to be related specifically to ventricular wall vibrations during rapid filling, and the spectra of the amplitude-frequency relation shifted toward the audible range with increases in diastolic pressure, wall stiffness or filling rate. Spectral analysis of S3 may be useful in assessing pathologic changes in myocardial wall properties.

Animals↗