Biomedical subjects

F Spinale

Publications and source records attributed to F Spinale.

5 recordsLinked to original sources

PubMed1993

Changes in diastolic function during development and correction of chronic LV volume overload produced by mitral regurgitation.

BACKGROUND: Mitral regurgitation (MR) causes an augmentation in left ventricular (LV) diastolic function, increasing early diastolic filling rate and decreasing LV stiffness. Whether these changes in diastolic function persist, return to normal, or become abnormal after mitral valve replacement (MVR) is unknown. METHODS AND RESULTS: Simultaneous LV echocardiography and catheterization studies were performed in six dogs in the baseline state (baseline), 3 months after creation of MR (chronic MR), and 3 months after MVR. Chronic MR caused LV dilation (end-diastolic dimension increased from 4.5 +/- 0.1 cm in baseline to 5.8 +/- 0.1 cm in chronic MR, p < 0.05) and eccentric LV hypertrophy (LV-to-body weight ratio increased from 3.6 +/- 0.2 g/kg in baseline to 4.9 +/- 0.4 g/kg in chronic MR, p < 0.05). Chronic MR caused an increase in LV early diastolic filling rate (peak rate of increase in minor-axis dimension increased from 11 +/- 1 cm/sec in baseline to 18 +/- 1 cm/sec in chronic MR, p < 0.05), did not change the time constant of myocardial relaxation (tau was 31 +/- 4 msec in baseline and 30 +/- 2 msec in chronic MR), and caused a decrease in the modulus of regional chamber stiffness from 7.7 +/- 1.2 in baseline to 2.4 +/- 0.03 in chronic MR, p < 0.05. MVR caused the resolution of LV dilation (end-diastolic dimension returned to normal [4.8 +/- 0.2 cm]), but three months after MVR, regression of LV hypertrophy was incomplete (LV-to-body weight ratio remained elevated [4.4 +/- 0.5 g/kg]). After MVR, LV early diastolic filling rate (8 +/- 1 cm/sec), the relaxation time constant (31 +/- 2 msec), chamber stiffness (7.1 +/- 1.8), myocardial stiffness (11.2 +/- 3.1), and LV end-diastolic pressure (8 +/- 1 mm Hg) returned to normal. CONCLUSIONS: The enhanced diastolic function seen in chronic MR returned to normal after correction of the chronic volume overload by MVR.

Animals↗

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↗

PubMed1991

Depressed contractile function due to canine mitral regurgitation improves after correction of the volume overload.

It is known that long-standing volume overload on the left ventricle due to mitral regurgitation eventually leads to contractile dysfunction. However, it is unknown whether or not correction of the volume overload can lead to recovery of contractility. In this study we tested the hypothesis that depressed contractile function due to volume overload in mitral regurgitation could return toward normal after mitral valve replacement. Using a canine model of mitral regurgitation which is known to produce contractile dysfunction, we examined contractile function longitudinally in seven dogs at baseline, after 3 mo of mitral regurgitation, 1 mo after mitral valve replacement, and 3 mo after mitral valve replacement. After 3 mo of mitral regurgitation (regurgitant fraction 0.62 +/- 0.04), end-diastolic volume had nearly doubled from 68 +/- 6.8 to 123 +/- 12.1 ml (P less than 0.05). All five indices of contractile function which we examined were depressed. For instance, maximum fiber elastance (EmaxF) obtained by assessment of time-varying elastance decreased from 5.95 +/- 0.71 to 2.25 +/- 0.18 (P less than 0.05). The end-systolic stiffness constant (k) was also depressed from 4.2 +/- 0.4 to 2.1 +/- 0.3. 3 mo after mitral valve replacement all indexes of contractile function had returned to or toward normal (e.g., EmaxF 3.65 +/- 0.21 and k 4.2 +/- 0.3). We conclude that previously depressed contractile function due to volume overload can improve after correction of the overload.

Animals↗

PubMed1987

The Blalock-Taussig shunt in infants: standard versus modified.

In recent years, the modified Blalock-Taussig shunt--a polytetrafluoroethylene graft from the subclavian artery to the pulmonary artery--has been preferred over the standard shunt by some surgeons because (1) it requires less dissection and (2) length of native vessels is not critical. From January, 1979, to June, 1985, we operated on 51 infants less than 1 year of age, including 26 less than 1 week of age, to palliate severe complex cyanotic congenital cardiac malformations. Twenty-four modified Blalock-Taussig shunts and 29 standard Blalock-Taussig shunts were created. The groups were concurrent. We reviewed all available cineangiograms and measured branch pulmonary and subclavian arteries. Pulmonary artery index was not different preoperatively in patients given a modified versus a standard Blalock-Taussig shunt (144 +/- 118 and 118 +/- 59 mm2/m2, respectively), but it was greater postoperatively in patients with a modified shunt (431 +/- 188 and 189 +/- 106 mm2/m2) (p = 0.07). Distortion of the pulmonary artery occurred less often after a modified Blalock-Taussig shunt (4/11) than a standard Blalock-Taussig shunt (6/8) (p = 0.06), though none of the distortions was severe. Early and late shunt failure occurred less often with a modified shunt (5/24) than with a standard shunt (15/29) (p less than 0.05). The modified Blalock-Taussig shunt had advantages over the standard Blalock-Taussig shunt in our series: pulmonary artery growth was greater, distortion of pulmonary arteries was less commonly seen, and shunt failure occurred less often. Thus, in infants, we believe the modified Blalock-Taussig shunt should be considered a reasonable alternative to the standard Blalock-Taussig shunt.

Blood Vessel Prosthesis↗

PubMed1986

Bovine pericardium for correction of congenital heart defects.

From July, 1980, until January, 1985, preserved bovine pericardium was utilized in the repair of a wide variety of congenital heart defects in 105 patients. Ages ranged from newborn to 56 years (mean, 9.6 years). Eighty-three of the 87 long-term survivors are in New York Heart Association Functional Class I or II. Bovine pericardium was not a contributing factor in the 12 hospital and 6 late deaths. The material was found to be flexible and easy to suture. No patient has demonstrated calcification of the patch in follow-up ranging from 6 to 60 months (mean, 30.2 months). Preserved bovine pericardium offers several potential advantages in the correction of congenital intracardiac defects.

Adolescent↗