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Percutaneous transluminal coronary angioplasty (PTCA) in complex coronary lesions (type B2 and C of the modified AHA/ACC classification) presents a lower primary success rate and higher risk of dissection than type A and B1 lesions. An alternative approach to this lesions is coronary rotational ablation (Rotablator, Heart Technology) with complementary PTCA using low inflation pressures ("facilitated angioplasty").Twenty-six type B2 and C lesions in 24 patients (pts) (8 female, 16 male, age 37-80 years) were treated with coronary rotational ablation and complementary PTCA between January 1993 and December 1994 (4.7% of all interventional coronary procedures performed in this period in our laboratory). Eleven pts had stable effort angina and 13 pts had unstable, class IB, IIB, and IIC, angina. The treated vessel was the LAD in 15 cases, CX in 5, RCA in 5, and an intermediate branch in one case. Coronary rotational ablation was proposed because of the presence of two or more risk factors for uneffective or complicated PTCA: eccentricity, calcified lesions, bifurcation stenosis, lesion length10 mm, severe stenosis (90-99%), ostial location and bend location (45-60 degrees). No lesion showed coronary thrombus, considered as absolute contraindication to coronary rotational ablation. We used small burrs (burr/artery ratio0.75), and complementary PTCA was performed using low inflation pressure (8 atm) and long balloons for long lesions (10 mm) in order to minimize the risk of dissection.Coronary rotational ablation was successfully performed in all but two cases (24/26; 92.3%), with a reduction of the stenosis from 88 +/- 9% to 45 +/- 10% (range 30-60%). In two pts (7.7%) the procedure was complicated by acute occlusion: both pts underwent effective salvage PTCA with 30% residual stenosis. Small type A and B dissections occurred in 4/26 cases (15.4%). All but one lesions complicated by acute occlusion or dissection following coronary rotational ablation were not or only slightly calcified. Complementary PTCA was performed in all but two pts who already presented 30% residual stenosis after rotational ablation. A further reduction of stenosis to 20 +/- 9% (range 5-30%) was achieved. After complementary PTCA four pts (15.4%) developed type A and B dissections; in one of these a Palmaz-Schatz stent was implanted, whereas the remaining three pts presented a residual stenosis below 30% and no further procedures were undertaken. Overall success rate of rotational atherectomy plus salvage or complementary PTCA or stenting was 100%, and no major complications (Q-wave myocardial infarction, emergency bypass surgery or death) occurred. Three pts showed delayed coronary run-off (slow reflow) after rotational ablation, and two of these released a small amount of cardiac specific enzymes (CK MB) without ECG changes and wall motion alteration on echocardiographic examination. Clinical restenosis, defined as recurrent angina and/or positive exercise stress test, developed in 45.8% (11 pts); in all these pts restenosis was angiographically evidenced (75-99%).Our experience suggests that coronary rotational ablation along with complementary PTCA using low inflation pressure and long balloons is safe and effective in type B2 and C lesions if calcifications are present; however, restenosis rate remains high.

Reversibility of pulmonary hypertension in patients affected by mitral stenosis is still under question.We selected 80 patients (mean age 48 +/- 14) who underwent successful percutaneous mitral valvuloplasty (PMV) for hemodynamic significant mitral stenosis (area1.5 cm2) with pulmonary hypertension (mean artery pulmonary pressure--PPM25 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--p0.001) 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.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, p0.01; systolic pulmonary pressure before PMV was 51.5 +/- 10.9 mm Hg vs 43.15 +/- 13.5 mm Hg after PMV--p0.01). 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).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.