Biomedical subjects

F Campisi

Publications and source records attributed to F Campisi.

4 recordsLinked to original sources

PubMed1996

Acute changes in left ventricular function after percutaneous transluminal mitral valvuloplasty.

Percutaneous balloon mitral valvuloplasty (PBMV) has been shown to induce an immediate increase in the left ventricular end-diastolic volume, which increase, in turn, has been attributed to an increase in left ventricular compliance. We studied 51 patients, 41 women and 10 men, who underwent PBMV, and were in sinus rhythm before and after the procedure. Heart rate did not vary significantly. There were increases in left ventricular end-diastolic volume (97.5 +/- 25.6 vs 112.7 +/- 25.7 ml/m2, P < 0.001), left ventricular end-diastolic pressure (8.7 +/- 3.0 vs 9.7 +/- 4.3 mmHg, P = 0.04), and both left ventricular systolic pressure and stress (118 +/- 20.5 vs 123 +/- 23.2 mmHg and 468 +/- 129 vs 580 +/- 164 mmHg; P = 0.04 and P < 0.001, respectively). The elastic stiffness constant did not vary (16.2 +/- 1.9 vs 15.7 +/- 1.9 (dimensionless units), P = 0.2). The increase in volume seemed to be particularly important when the ventricle appeared to be "shrunken" before PBMV. This increase was still present after a 1 year follow up. Thus, PBMV determines an increase in both end-diastolic volume and pressure, so that the left ventricle appears to move along a single pressure-volume curve. This enlargement evokes the Frank Starling mechanism, and improves systolic performance. Since it is still evident after a 1 year follow up, some concern may arise when a simultaneous volume overload is present, as in aortic insufficiency.

Adult↗

PubMed1995

[Percutaneous mitral valvuloplasty: the immediate and long-term results].

BACKGROUND: Between December 1988 and December 1992, 235 patients (pts) underwent percutaneous balloon mitral valvuloplasty (PBMV). METHODS AND RESULTS: There were 55 men (23%) aged 49 +/- 13 years and 180 women (77%) aged 51 +/- 13 years. Previous surgical commissurotomy (PSC) had been performed in 22 pts. Procedure was successful (area > 1.5 cm2 or area increase > or = 50% without mitral regurgitation > 2+) in 91.9% of pts, with increase in mitral valve area from 1.05 +/- 0.2 to 2.26 +/- 0.6 cm2, decrease of transvalvular mean pressure gradient from 14.4 +/- 5.5 to 6.05 +/- 4.91 mm Hg and increase of cardiac index from 2.79 +/- 0.75 to 3.17 +/- 0.9 l/m'/m2 (p < 0.001). Insufficient increase in valve area occurred in 3.8% of pts. Major complications included 5 pts with 3+ mitral regulation (MR) requiring mitral valve replacement (MVR), 2 TIA's (0.85%) and 1 pericardiocentesis (0.42%). At follow-up (mean 18.9 months) clinical improvement was achieved in 93.8% of pts (NYHA class from 2.4 to 1.3); mitral valve area was 1.9 +/- 0.4 cm2 and mean mitral valve gradient 5.3 +/- 2.3 mm Hg. Restenosis (area < 1.5 cm2 or > or = 50% loss of initial gain) occurred in 24 pts (10.16%). Six pts required MVR; 1 pt underwent a second successful PBMV. Multivariate study (logistic regression) identified as independent factors of severe MR NYHA class and PSC; echo score, age and basal mean mitral valve gradient were independent factors for restenosis. CONCLUSIONS: In conclusion, PBMV is a safe technique and stable clinical improvement can be obtained in the majority of pts.

Adolescent↗

PubMed1994

Measurement of systemic resistances in aortic regurgitation.

Peripheral resistance is usually measured by dividing mean aortic pressure by mean aortic flow. This statement holds true as long as resistance is constant throughout the heart cycle. This is not the case in aortic regurgitation, because during diastole, but not in systole, a conduit is opened to blood flow through the regurgitating valve. Peripheral resistance was measured in 11 patients with aortic regurgitation and in 23 normal subjects by solving for Ri in the "windkessel" equation. We compared this resistance (R1) with that measured by standard methods (RES). In normal subjects, R1 and RES are almost identical [R1 = 0.96 (RES) +/- 0.12, r = .95], while in aortic regurgitation there is no correlation [R1 = 0.64 (RES) +/- 1.4, r = 0.2]. RES in normal subjects is increased with respect to RES in aortic regurgitation (32 vs 22, p = 0.0019), while R1 in aortic regurgitation is decreased compared to both R1 and RES in normal subjects (13.5 vs 21 and 22, p = 0.0063). The difference between R1 and RES in aortic regurgitation is related to the regurgitating volume. Compliance, calculated by assuming a monoexponential diastolic aortic pressure decay, is markedly decreased in aortic insufficiency, while it is increased if it is calculated by dividing the time constant of aortic pressure decay by R1. Thus, in severe aortic regurgitation peripheral resistance is usually less than normal, and standard methods of measurement fail to detect this fact. Correct evaluation of resistance and compliance may be useful to evaluate ventriculoarterial coupling and to titrate vasodilator therapy in this disease.

Aortic Valve Insufficiency↗

PubMed1994

[Regression of pulmonary hypertension in mitral stenosis: an echo-hemodynamic study in patients who underwent mitral balloon valvuloplasty].

BACKGROUND: Reversibility of pulmonary hypertension in patients affected by mitral stenosis is still under question. METHODS: We selected 80 patients (mean age 48 +/- 14) who underwent successful percutaneous mitral valvuloplasty (PMV) for hemodynamic significant mitral stenosis (area < 1.5 cm2) with pulmonary hypertension (mean artery pulmonary pressure--PPM > 25 mm Hg), producing significant increase in mitral valve area (area before PMV = 0.99 +/- 0.23 cm2 vs 2.08 +/- 0.32 cm2 after PMV--p < 0.001) without hemodynamic complications (mitral insufficiency and/or interatrial shunt). Cardiac index, pulmonary arterial pressures, and pulmonary arteriolar resistances were invasively evaluated before and immediately after valvuloplasty. Systolic pulmonary pressure was indirectly monitored by Doppler method in a period from 1 to 3 months after percutaneous mitral valvuloplasty. RESULTS: In general (70 pts.) there was an immediate significant reduction of pulmonary pressure after percutaneous mitral valvuloplasty (mean pulmonary pressure before PMV was 33.9 +/- 7.9 mm Hg vs 26.8 +/- 9.5 mm Hg after PMV, p < 0.01; systolic pulmonary pressure before PMV was 51.5 +/- 10.9 mm Hg vs 43.15 +/- 13.5 mm Hg after PMV--p < 0.01). A small subgroup of 10 pts., older in age (mean 59 +/- 15), manifested no reduction of pulmonary pressure immediately after procedure (mean pulmonary pressure before PMV = 35.2 +/- 8.37 mm Hg vs 36.5 +/- 6 mm Hg after PMV, p: ns; systolic pulmonary pressure before PMV = 58.2 +/- 10.6 mm Hg vs 59.2 +/- 9.6 mm Hg. after PMV, p: ns) and 4 of them (mean age 65 +/- 15) persisting pulmonary hypertension at 1-3 months follow-up (systolic pulmonary pressure before PMV = 58.75 +/- 14 mm Hg, immediately after PMV = 57.8 +/- 12.5 mm Hg, and 1-3 months after PMV = 62.5 +/- 9 mm Hg--p: ns). CONCLUSIONS: Neither severe pulmonary hypertension, nor pulmonary arteriolar resistances but only age seems to be a predictive factor of persisting pulmonary hypertension after percutaneous mitral valvuloplasty in mitral stenosis.

Adolescent↗