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Biomedical subjects

B A Carabello

Publications and source records attributed to B A Carabello.

At least 19 recordsLinked to original sources
PubMed1992

The changing unnatural history of valvular regurgitation.

In the past 15 years three major advancements have improved the lot of our patients with left-sided valvular regurgitation. First, the concept that mitral and aortic regurgitation were similar volume overloading lesions has changed. Mitral regurgitation constitutes a nearly pure volume overload wherein the excess volume is ejected against relatively low pressure into the left atrium. On the other hand, aortic regurgitation represents a combined pressure and volume overload in which the excess volume being pumped is ejected against the relatively high pressure of the aorta. These differences in loading between mitral and aortic regurgitation produce a different response to operation. Afterload reduction after correction of aortic regurgitation increases ejection performance if it was decreased preoperatively. Conversely, afterload increases after mitral valve replacement, decreasing ejection performance. These differences make the left ventricle in mitral regurgitation less tolerant of preoperative dysfunction than the left ventricle in aortic regurgitation. Second, with respect to aortic regurgitation, reproducible indexes have been developed that identify when left ventricular dysfunction is present, leading to earlier operation in an attempt to avoid permanent ventricular dysfunction. In turn, earlier operation has led to a fall in operative mortality rate and an almost universal increase in left ventricular function if it was depressed preoperatively. Third, with regard to mitral regurgitation, recognition of the importance of the mitral valve apparatus in maintaining left ventricular function has led to an increased emphasis on chordal preservation during mitral valve operations.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve Insufficiency↗
PubMed1992

Left ventricular volume determined echocardiographically by assuming a constant left ventricular epicardial long-axis/short-axis dimension ratio throughout the cardiac cycle.

OBJECTIVES: The purpose of this study was to develop and test a simplified echocardiographic method to calculate left ventricular volume. BACKGROUND: This method was based on the assumption that the ratio of the left ventricular epicardial long-axis dimension to the epicardial short-axis dimension was constant throughout the cardiac cycle. With use of this constant ratio, the method developed to calculate left ventricular volume at a given point in the cardiac cycle required the left ventricular endocardial long-axis dimension to be measured at only one point in the cardiac cycle. METHODS: Studies were performed in 13 normal dogs, 8 normal puppies, 9 normal pigs, 12 dogs with aortic stenosis, 13 dogs with acute mitral regurgitation, 12 dogs with chronic mitral regurgitation, 7 dogs that had undergone mitral valve replacement and 6 pigs that had had chronic supraventricular tachycardia. Animals with aortic stenosis developed left ventricular pressure overload hypertrophy with a 60% increase in left ventricular mass; chronic mitral regurgitation caused left ventricular volume overload hypertrophy with a 46% increase in left ventricular volume; supraventricular tachycardia caused a dilated cardiomyopathy with a 55% decrease in left ventricular ejection fraction. RESULTS: The left ventricular epicardial long-axis/short-axis dimension ratio remained constant throughout the cardiac cycle in each animal group. End-diastolic and end-systolic volumes calculated with the simplified echocardiographic method correlated closely with angiographically measured volumes; for end-diastolic volume, echocardiographic end-diastolic volume = 1.0 (angiographic end-diastolic volume) -1.8 ml, r = 0.96; for end-systolic volume, echocardiographic end-systolic volume = 0.98 (angiographic end-systolic volume) -0.7 ml, r = 0.95. CONCLUSIONS: Thus the left ventricular epicardial long-axis/short-axis dimension ratio was constant throughout the cardiac cycle in a variety of animal species and age groups and in the presence of cardiac diseases that significantly altered left ventricular geometry and function. The simplified echocardiographic method examined provided an accurate determination of left ventricular volumes.

Animals↗
PubMed1992

Aortic valve resistance as an adjunct to the Gorlin formula in assessing the severity of aortic stenosis in symptomatic patients.

OBJECTIVES: This study was conducted to determine the utility of aortic valve resistance in assessing the severity of aortic stenosis. BACKGROUND: Assessment of the severity of aortic stenosis has traditionally employed hemodynamic data and the Gorlin formula to calculate the area of the aortic valve. Recently, flow dependence of the Gorlin formula has been identified and the accuracy of the formula challenged. Aortic valve resistance, the quotient of gradient and cardiac output, has been advanced as potentially useful in assessing the severity of valve stenosis. METHODS: We studied 48 symptomatic patients with an initial diagnosis of severe aortic stenosis based on a calculated aortic valve area of less than or equal to 0.8 cm2 by the Gorlin formula. Forty of these patients (Group I) were confirmed to have severe aortic stenosis, whereas 8 (Group II) were subsequently proved not to have severe aortic stenosis. The 18 patients in Group I with a valve area of 0.6 to 0.8 cm2 (Group IA) were directly compared with Group II patients who had a similar valve area. RESULTS: Aortic valve area was nearly identical in Group IA and Group II patients (0.69 +/- 0.05 and 0.71 +/- 0.06 cm2, respectively, p = NS). However, aortic valve resistance was much less in Group II patients (212 +/- 6 vs. 316 +/- 11 dynes.s.cm-5, p less than 0.0001). In this small cohort, aortic valve resistance achieved nearly complete separation of patients in Groups IA and II. CONCLUSIONS: In some patients with relatively mild aortic stenosis, the calculated valve area may indicate that the stenosis is severe. The use of aortic valve resistance in conjunction with the Gorlin formula helps separate patients with truly severe aortic stenosis from those with milder disease.

Aged↗
PubMed1992

Left ventricular hypertrophy in a canine model of reversible pressure overload.

OBJECTIVE: The goal of therapy for left ventricular pressure overload should include regression of the associated left ventricular hypertrophy, but this process is incompletely understood. The aim of the study was to characterise the extent and time course of the progression and regression of pressure overload left ventricular hypertrophy in a canine hypertrophy model. METHODS: Six puppies were studied longitudinally with haemodynamic and echocardiographic measurements for 10 months. The study animals underwent ascending aortic banding at nine weeks of age which produced an initial gradient of 30 mm Hg. Subsequent growth led to an increase in gradient and the development of left ventricular hypertrophy. Then thoracotomy was again performed to remove the band. One month later, balloon aortoplasty was performed to remove the residual gradient. The animals were then observed for six months. RESULTS: Growth increased the gradient to 105(SEM 10) mm Hg three months after banding. The left ventricular weight to body weight ratio (g.kg-1), an index of hypertrophy, was 7.2(0.5) after three months of pressure overload. Subsequently the band was surgically removed, reducing the gradient to an average of 58(10) mm Hg. Balloon dilatation of the residual aortic stricture reduced the gradient further to 6(5) mm Hg. Over the ensuing six months, echocardiographic determination of left ventricular mass showed the regression in left ventricular hypertrophy. After six months, left ventricular weight to body weight ratio in the previously banded animals was significantly reduced from 7.2(0.5) to 5.3(0.2) (p less than 0.05). CONCLUSIONS: The model produced over 100% left ventricular hypertrophy, most of which regressed following removal of the pressure overload.

Angioplasty, Balloon↗
PubMed1992

Left ventricular hypertrophy due to volume overload versus pressure overload.

Left ventricular hemodynamic overload produces an increase in stroke work (SW), which is compensated by the development of left ventricular hypertrophy. However, recent reports question the adequacy of this compensation in mitral regurgitation (MR). Accordingly, we examined the adequacy of compensatory hypertrophy in chronic experimental MR. Six dogs with chronic severe MR were matched according to SW with six dogs that had severe chronic aortic stenosis (ASSW). SW in the two groups was increased identically (40%) compared with normals. However, the hypertrophic response was much greater in the AS group [left ventricular wt (g) to body wt (kg) ratio (LVBW) 4.0 +/- 0.2 normals, 5.0 +/- 0.2 MR, and 7.5 +/- 0.2 ASSW; P < 0.05 MR vs. ASSW]. This differing hypertrophic response increased normalized SW, the area within the stress-volume loop, in MR (90 +/- 5 g) vs. 63 +/- 5 g in ASSW (P < 0.05). Thus in MR, each unit of myocardium had to perform more work than in AS. In a separate comparison, four different dogs with AS (ASHy), which had a similar amount of hypertrophy to the MR dogs (LVBW) (5.0 +/- 0.2 MR, 5.2 +/- 0.2 ASHy) were studied. SW was greater in the MR group, suggesting more SW overload was required to produce similar amounts of hypertrophy in MR vs. AS. Contractile function was depressed in the MR group but not in the AS. These findings indicate that the hypertrophic response to a similar SW demand is less in MR than AS, a response associated with contractile dysfunction in the MR group.

Animals↗
PubMed1992

Mitral valve replacement with and without chordal preservation in patients with chronic mitral regurgitation. Mechanisms for differences in postoperative ejection performance.

BACKGROUND: Standard mitral valve replacement (MVR) in patients with chronic mitral regurgitation consistently results in a decrease in postoperative left ventricular (LV) ejection performance. This fall in ejection performance has been attributed, at least in part, to unfavorable loading conditions imposed by the elimination of the low-impedance pathway for LV emptying into the left atrium. In contrast to standard MVR in which the chordae tendineae are severed, however, MVR with chordal preservation (MVR-CP) does not usually decrease LV ejection performance despite similar removal of the low-impedance pathway. The purpose of the present study was to define the mechanisms responsible for this discordance in postoperative ejection performance between MVR with and without chordal preservation. METHODS AND RESULTS: Echocardiography and sphygmomanometer blood pressures were obtained in 15 patients with pure chronic mitral regurgitation before and 7-10 days after mitral valve surgery. These measurements were used to calculate ventricular volume, wall stress, and ejection fraction. Seven patients underwent MVR with chordal transection (MVR-CT), and eight patients underwent MVR-CP. MVR-CT resulted in no postoperative change in LV end-diastolic volume, a significant increase in LV end-systolic volume, a significant increase in end-systolic stress, from 89 +/- 9 to 111 +/- 12 g/cm2 (p < 0.05), and a significant decrease in ejection fraction, from 0.60 +/- 0.02 to 36 +/- 0.02 (p < 0.05). In contrast, patients who underwent MVR-CP had a significant decrease in LV end-diastolic and end-systolic volumes. End-systolic wall stress actually fell from 95 +/- 6 to 66 +/- 6 g/cm2 (p < 0.05), and ejection fraction was unchanged (0.63 +/- 0.01 before and 0.61 +/- 0.02 after mitral valve surgery) instead of reduced. CONCLUSIONS: MVR-CT resulted in a decrease in ejection performance caused in part by an increase in end-systolic stress, which in turn increased end-systolic volume. Conversely, MVR-CP resulted in a smaller LV size, allowing a reduced end-systolic stress and preservation of ejection performance despite closure of the low-impedance left atrial ejection pathway.

Chordae Tendineae↗
PubMed1992

Cellular and ventricular contractile dysfunction in experimental canine mitral regurgitation.

This study was designed to answer two questions. First, does the left ventricular contractile dysfunction resulting from mitral regurgitation (MR) reflect a primary defect in the cardiac muscle cell? Second, what is the basis for any change in cellular contractile function that might be observed? Left ventricular volume overload was produced in 10 dogs by catheter transection of mitral chordae tendineae. Three months later in these and in seven control dogs, left ventricular contractile function was characterized by the end-ejection stress-volume relation (EESVR). Investigators who were blinded to these results then characterized the contractile performance of cardiac muscle cells, or cardiocytes, from these same left ventricles in terms of the viscosity (graded external load)-velocity relation. Finally, the tissue and cellular components of these same left ventricles were analyzed morphometrically. Both the left ventricles from the MR group and their constituent cardiocytes showed marked contractile abnormalities. By matching ventricles with cells from the same MR dogs, ventricular EESVR was correlated with cardiocyte peak sarcomere shortening velocity (SSV). The correlation coefficient between EESVR and SSV was 0.63, but between a size-independent measure of active ventricular stiffness and SSV, it was 0.88. No change in left ventricular interstitial volume fraction was found in MR dogs, but both ventricular and cellular contractile dysfunction strongly correlated with a decreased volume fraction of cardiocyte myofibrils. Last, in an attempt to relate the degree of contractile dysfunction to the hypertrophic response, left ventricular mass in the MR dogs was correlated with both cellular and ventricular contractile indexes; no significant correlation was found. Three conclusions are warranted by these studies. First, chronic left ventricular volume overload from mitral regurgitation leads to contractile defects at both the ventricular and cellular levels, the extent of which correlates well in individual animals. Second, no quantitative interstitial change resulted from MR. Taken together, these two findings strongly suggest that the contractile defect is intrinsic to the cardiocyte. Third, while the contractile abnormality in MR remains undefined, the most basic defects appear to be a combination of myofibrillar loss with the failure of compensatory hypertrophy to occur in response to progressive decrements in cellular and ventricular function.

Animals↗
PubMed1992

Coronary blood flow after the regression of pressure-overload left ventricular hypertrophy.

Abnormal coronary blood flow (CBF) in long-standing left ventricular (LV) pressure-overload hypertrophy has been associated with ischemia and LV dysfunction. Thus, goals of therapy in pressure overload are not only the relief of the overload itself but also regression in hypertrophy and subsequent improvement in CBF. However, little is known about CBF in humans or in large mammals after the relief of pressure overload, when the hypertrophy has regressed. This study was performed to test the hypothesis that, even 6 months after the relief of pressure overload in the dog, CBF would still be abnormal. Three groups of dogs were studied: 1) normal control dogs (NL group), 2) dogs with LV pressure-overload hypertrophy (LVH group), and 3) dogs that had developed LV pressure-overload hypertrophy but in whom the pressure overload was relieved 6 months before the final study (LVH Reg group). CBF was studied in conscious dogs by use of the radiolabeled microsphere technique at rest, during rapid atrial pacing, and during maximum coronary vasodilation produced by adenosine infusion. The ratio of LV weight (g) to body weight (kg) (LVBW) was 4.2 +/- 0.3 in the NL group, 7.1 +/- 0.6 in the LVH group, and 7.7 +/- 0.5 in the LVH Reg group before pressure-overload relief (p = NS, LVH versus LVH Reg). Six months after removal of the pressure overload, the LVBW in the LVH Reg group had fallen to 5.5 +/- 0.3 (p < 0.05), but this LVBW was still greater than that in the NL group (p < 0.05). During rapid atrial pacing, endocardial and epicardial CBF rose significantly in NL dogs. However, during rapid atrial pacing, endocardial CBF fell from 1.18 +/- 0.22 to 0.7 +/- 0.20 ml/min per gram in the LVH group (p < 0.05) and did not rise in the LVH Reg group. During adenosine infusion, endocardial blood flow increased in NL dogs from 1.63 +/- 0.13 to 4.0 +/- 0.3 ml/min per gram and increased to a similar level in the LVH Reg group. Although CBF increased during adenosine infusion in the LVH group, the increase was less than that in the NL or LVH Reg group (p < 0.05). Minimum coronary vascular resistance was similar in NL dogs (14 +/- 2 units) and LVH Reg dogs (18 +/- 3 units, p = NS) but was significantly elevated (32 +/- 10 units) in LVH dogs (p < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine↗
PubMed1992

Left ventricular mechanics and myocyte function after correction of experimental chronic mitral regurgitation by combined mitral valve replacement and preservation of the native mitral valve apparatus.

BACKGROUND: Contractile function improves after correction of experimental mitral regurgitation, but ejection performance becomes depressed when mitral valve replacement involves chordal transection. A role for chordal transection in producing the depressed ejection performance was suspected but uncertain. Therefore, in this study, we tested two specific hypotheses: 1) that contractile function would improve and, in conjunction with chordal preservation, would allow for preserved ejection performance and 2) that improved left ventricular contractile function after surgery would be reflected in the function of myocytes isolated from the affected left ventricles. METHODS AND RESULTS: We examined ventricular contractile function and ejection performance and isolated myocyte function after correction of experimental mitral regurgitation (chordal rupture) with mitral valve replacement that involved chordal preservation. After 3 months of chronic mitral regurgitation, the average regurgitant fraction of seven dogs was 0.77 +/- 0.04. End-diastolic volume had increased from 79 +/- 5 to 132 +/- 10 cm3 (p < 0.05). At that time, all indexes of left ventricular contractile function were depressed. Three months after mitral valve replacement with chordal preservation, end-diastolic volume fell to 100 +/- 4 cm3 (p < 0.05). At this time, all indexes of contractile function had returned to normal. End-systolic stress and ejection fraction after mitral valve replacement were similar to their baseline levels. Viscosity-velocity curves (analogous to force-velocity curves) of myocytes isolated from the affected left ventricles were similar to those of myocytes isolated from normal left ventricles. CONCLUSIONS: We conclude that mitral valve replacement with chordal preservation allows ventricular contractile function to return to normal. Normal global ventricular function, in turn, is associated with normal function of the individual myocytes that compose the left ventricular chamber. Further, chordal preservation allowed for loading and ejection performance to return to premorbid levels.

Animals↗
PubMed1991

Effects of left ventricular volume overload produced by mitral regurgitation on diastolic function.

We hypothesized that the left ventricle's ability to compensate for the volume overload produced by mitral regurgitation (MR) depends, at least in part, on associated changes in left ventricular (LV) diastolic function. Indexes of the rate of LV pressure decline, the rate and extent of early diastolic filling, and LV diastolic stiffness were measured with simultaneous echocardiography and catheterization in the baseline state (baseline), immediately after creation of MR (acute MR), and 3 mo after creation of MR (chronic MR). Data are means +/- SD. MR caused LV dilation; end-diastolic dimension increased from 4.3 +/- 0.4 in baseline to 4.7 +/- 0.5 in acute MR and 5.8 +/- 0.1 cm in chronic MR (P less than 0.05 vs. baseline for both). Chronic MR caused eccentric LV hypertrophy; LV-to-body weight ratio increased from 3.6 +/- 0.3 in baseline to 4.5 +/- 0.2 g/kg in chronic MR (P less than 0.05 vs. baseline). Acute MR increased LV end-diastolic pressure from 8 +/- 4 in baseline to 15 +/- 3 mmHg (P less than 0.05 vs. baseline); chronic MR did not further increase LV end-diastolic pressure (14 +/- 4 mmHg). MR increased the transmitral pressure gradient from 5 +/- 1 in baseline to 14 +/- 3 in acute MR and 20 +/- 6 mmHg in chronic MR (P less than 0.05 vs. baseline for both). MR increased LV early diastolic filling rate; peak rate of increase in minor axis dimension increased from 11 +/- 2 baseline to 18 +/- 2 in acute MR and 19 +/- 2 cm/s in chronic MR (P less than 0.05 vs. baseline for both). Acute MR did not change LV stiffness constants. Chronic MR decreased LV stiffness; the modulus of chamber stiffness decreased from 7.1 +/- 2.8 in baseline to 2.9 +/- 1.6 in chronic MR (P less than 0.05 vs. baseline). Thus MR caused compensatory changes in LV diastolic function. These changes resulted from an increased transmitral pressure gradient and increased LV distensibility.

Animals↗
PubMed1991

Coronary blood flow in dogs with contractile dysfunction due to experimental volume overload.

BACKGROUND: Abnormalities in coronary blood flow are responsible for stress-induced reductions in contractile function in pressure overload hypertrophy. Less is known about coronary blood flow in volume overload. In this study, we tested the hypothesis that coronary blood flow abnormalities were responsible for contractile abnormalities in experimental volume overload hypertrophy. METHODS AND RESULTS: We examined coronary blood flow at rest and during pacing in seven dogs with contractile dysfunction secondary to chronic experimental mitral regurgitation (average regurgitant fraction at 3 months, 0.58 +/- 0.05). After 3 months of mitral regurgitation, left ventricular mass had increased from 92 +/- 8 g at baseline to 118 +/- 10 g (p less than 0.002). The slope of the end-ejection stress-volume relation, one of our indexes used to estimate contractile function, had fallen from 5.4 +/- 0.3 at baseline to 3.0 +/- 0.3 at 3 months of mitral regurgitation (p less than 0.001). In the mitral regurgitation dogs, coronary blood flow at rest was similar to that of control dogs (endocardial blood flow: control dogs, 1.33 +/- 0.12 ml/min/g; mitral regurgitation dogs, 1.16 ml/min/g, p = NS; epicardial blood flow at rest: control dogs, 1.30 +/- 0.16 ml/min/g; mitral regurgitation dogs 1.13 +/- 0.2 ml/min/g, p = NS). With pacing-induced stress, coronary blood flow increased appropriately in control and mitral regurgitation dogs. Ultrasonic dimension gauges placed in the endocardium and epicardium demonstrated no further deterioration in ventricular function during pacing in the mitral regurgitation dogs. In a separate group of five control dogs and five dogs with mitral regurgitation and left ventricular dysfunction, coronary blood flow was examined in the conscious closed-chest state at rest, during adenosine infusion, and during rapid atrial pacing (240 beats/min). Blood flow increased similarly in both groups during pacing and adenosine infusion. CONCLUSIONS: We conclude that in dogs with mitral regurgitation that have developed contractile dysfunction, abnormalities in coronary blood flow do not explain the resting contractile dysfunction. Furthermore, studies during pacing-induced stress and coronary vasodilation with adenosine demonstrate that substantial coronary blood flow reserve is present in this type of volume overload hypertrophy.

Animals↗
PubMed1991

Anesthetic and postoperative protocols for a canine model of reversible left ventricular volume overload.

The purpose of this study was to develop anesthetic and postoperative methods that could be used in a canine model of reversible left ventricular volume overload (LVVO). LVVO was created by inducing mitral regurgitation (MR) in adult conditioned dogs. Using fluoroscopy, MR was induced by passing urologic grasping forceps into the left ventricle through a carotid artery and rupturing one or more chordae tendinea. Cardiac catheterization was performed after significant cardiac dysfunction developed (3 months after creation of MR) in order to collect data to confirm reduced contractile function. The MR was repaired by replacing the damaged valve with a bovine pericardial xenograft. Dogs were followed with sequential cardiac catheterizations to determine if the valvular replacement reversed the cardiac dysfunction. To develop this model, unique anesthetic and post-operative care protocols had to be instituted. In order not to exacerbate the existing cardiac dysfunction, a high dose narcotic anesthetic regimen using a sufentanil infusion at 9-13 microgram/kg h-1 was developed in association with cardiopulmonary bypass and hypothermia for the mitral valve replacement surgery. Intensive postoperative care protocols that involved major personnel and pharmaceutic interventions were necessary. Using our methods 11/17 dogs survived the procedure and were included in the protocol for study of mechanisms involved in reversal of cardiac dysfunction.

Anesthesia↗
PubMed1991

Ventricular failure and cellular remodeling with chronic supraventricular tachycardia.

Chronic supraventricular tachycardia has been associated with ventricular dysfunction in human beings and in animals. The changes in ventricular size and shape and the myocyte remodeling that may occur with chronic supraventricular tachycardia are unknown. Left and right ventricular remodeling and myocyte changes were examined in 12 pigs after 3 weeks of atrial pacing (supraventricular tachycardia at 240 beats/min and in 10 control pigs (105 +/- 3 beats/min). Chronic supraventricular tachycardia resulted in decreased left ventricular and right ventricular ejection fractions compared with control values (left ventricle, 26% +/- 4% versus 60% +/- 1%; right ventricle, 19% +/- 3% versus 53% +/- 3%; p less than 0.05 for both), decreased wall thickness (left ventricle, 8.3 +/- 0.1 mm versus 10.5 +/- 0.2 mm; right ventricle, 2.8 +/- 0.3 mm versus 4.2 +/- 0.2 mm; p less than 0.05 for both), and increased end-diastolic volumes (left ventricle, 66 +/- 10 ml versus 54 +/- 4 ml; right ventricle, 78 +/- 8 ml versus 56 +/- 4 ml; p less than 0.05 for both). Myocardial water content was significantly higher with supraventricular tachycardia than in control pigs (left ventricle, 82% +/- 4% versus 76% +/- 4%; right ventricle, 83% +/- 4% versus 78% +/- 2%; p less than 0.05 for both). According to computer-aided stereological studies, the percent volume of myocytes in the subendocardial layer of the hearts that underwent supraventricular tachycardia was smaller than that of the control hearts (left ventricle, 62% +/- 2% versus 79% +/- 1%; right ventricle, 55% +/- 4% versus 77% +/- 1%; p less than 0.05 for both) and myocyte diameter was reduced (left ventricle, 16 +/- 1 microns versus 23 +/- 2 microns; right ventricle, 13 +/- 1 microns versus 22 +/- 2 microns; p less than 0.05 for both). Further, myocytes isolated from the left ventricles of the group with supraventricular tachycardia were significantly longer than were control myocytes (190 +/- 25 microns versus 145 +/- 30 microns, p less than 0.05 for both). In summary, chronic supraventricular tachycardia caused significant right and left ventricular failure, with a reduction in wall thickness and chamber dilatation. This was accompanied by a reduction in the percent volume of myocytes occupying the subendocardial layer, with reduced myocyte diameter and increased myocyte length and water content. These changes are likely to be important in understanding supraventricular tachycardia-induced ventricular dysfunction.

Animals↗
PubMed1991

Timing of surgery in mitral and aortic stenosis.

This article reviews the indications and contraindications for the surgical correction of mitral and aortic stenosis. Ventricular mechanics and pathophysiology of both diseases are reviewed and related to the development of symptoms. New aspects of the hemodynamic evaluation and controversies associated with mitral and aortic stenosis are highlighted.

Aged↗
PubMed1990

Relationship between bioimpedance, thermodilution, and ventriculographic measurements in experimental congestive heart failure.

PURPOSE OF INVESTIGATION - Bioimpedance cardiography has been suggested as a non-invasive means to monitor cardiac function but has not been tested in cases of severe ventricular dysfunction. This study compared thermodilution stroke volume, ventriculographic left ventricular ejection fraction, bioimpedance stroke volume, and the maximum first derivative of the bioimpedance signal dZ/dtmax, during the development of experimental congestive heart failure. DESIGN - Simultaneous thermodilution stroke volume, ventriculography, and bioimpedance measurements were serially measured in pigs following acute pacing, and after 1, 2, and 3 weeks of tachycardia. Thermodilution stroke volume measurements were obtained by positioning a thermistor tipped catheter into the pulmonary artery and integrating the thermodilution curve with respect to heart rate. Left ventricular stroke volume and ejection fractions were measured from single plane ventriculograms using the area-length method. Using a series of electrodes positioned on the thoracic segment and a low level current (2.5 ma), the bioimpedance waveform was recorded and stroke volume and dZ/dtmax computed. SUBJECTS - The subjects were eight pigs (23-30 kg) with developing ventricular dysfunction due to chronic rapid atrial pacing (240 beats.min-1) and four controls. MEASUREMENTS AND MAIN RESULTS - Left ventricular ejection fraction decreased significantly from acutely paced values following 7 d tachycardia [60(SEM 1)% v 41(3)% respectively, p less than 0.01] and continued to decline with longer durations of tachycardia. A significant correlation was observed between ejection fraction and dZ/dtmax (r = 0.74, n = 32). Thermodilution and bioimpedance stroke volumes fell significantly from acutely paced values after week 2 of tachycardia [thermodilution: 13.8(0.9) v 8.5(1.4) ml; bioimpedance: 13.6(1.1) v 11.2(1.5) ml respectively, p less than 0.05] and were highly correlated throughout the study period (r = 0.90, n = 32). However, bioimpedance overestimated thermodilution values at week 2 (p less than 0.05) and at week 3 of tachycardia [thermodilution: 8.4(0.8) ml v bioimpedance: 9.6(1.0) ml, NS]. CONCLUSION - In a tachycardia induced model of heart failure, bioimpedance was significantly correlated with thermodilution stroke volume. The peak first derivative of the bioimpedance signal dZ/dtmax may provide a non-invasive index of ventricular pump performance. While these results are promising, further studies are required to evaluate the diagnostic value of bioimpedance cardiography in the clinical setting.

Animals↗
PubMed1990

Wavefront myocyte injury and relationship to function in right ventricular ischemia.

Past studies of acute canine right ventricular (RV) ischemia have failed to demonstrate early irreversible injury or decreased function. However, the dog frequently has an extensive collateral circulation not found in all humans. The aim of this study was to measure RV global and regional function after right coronary occlusion in 32 closed-chest pigs. RV function was assessed by biplane ventriculography, and myocardial injury was examined by immunohistochemical localization of creatine kinase (CK) and by electron microscopy. Global RV ejection fraction and apical and midventricular regional function declined significantly after 10 min of occlusion. Injury to the myocardium progressed from the endocardium to the epicardium. Significant injury was observed in myocytes of the endocardium, midmyocardium, and epicardium at 10, 30, and 60 min of occlusion, respectively. Regional RV function and the extent of myocardial injury showed a high correlation (r = 0.96, P less than 0.01). The strong CK immunostaining seen in control hearts was diminished in myocytes along the endocardium at 15 min of occlusion. Depletion of immunoreactive CK in myocytes progressed toward the epicardium with longer ischemic times. These findings demonstrate that RV ischemic injury progresses in a wavefront fashion in the pig, which has similar coronary anatomy to humans, and irreversible myocardial injury occurred after 15-30 min of ischemia.

Animals↗