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Dual antiplatelet therapy improves angiographic results of primary percutaneous coronary intervention (pPCI) in patients with STEMI. The new oral P2Y12 inhibitors (P2Y12-I) prasugrel and ticagrelor are the gold-standard drugs because of a faster and more intense effect when compared to clopidogrel.

Objectives The aim of this trial was to compare cutting balloon angioplasty (CBA) with conventional balloon angioplasty (i.e., percutaneous transluminal coronary angioplasty [PTCA]) for the treatment of patients with coronary in-stent restenosis (ISR). Background Retrospective studies suggest CBA might be superior to conventional PTCA in the treatment of ISR. Methods The Restenosis Cutting Balloon Evaluation Trial (RESCUT) is a multicenter, randomized, prospective European trial including 428 patients with all types of ISR (e.g., focal, multifocal, diffuse, proliferative). Results In both groups, the majority of ISR lesions were shorter than 20 mm. The length of restenotic stents was similar (CBA: 18.6 ± 9.7 mm; PTCA: 18.3 ± 8.7 mm). The number of balloons used to treat ISR was lower in the CBA group: only one balloon was used in 82.3% of CBA cases, compared with 75% of PTCA procedures (p = 0.03). Balloon slippage was less frequent in the CBA group (CBA 6.5%, PTCA 25%; p Conclusions Cutting balloon angioplasty did not reduce recurrent ISR and major adverse cardiac events, as compared with conventional PTCA. However, CBA was associated with some procedural advantages, such as use of fewer balloons, less requirement for additional stenting, and a lower incidence of balloon slippage.

Background: The goal of STEMI treatment is early reperfusion. The new oral P2Y12 inhibitors (P2Y12-I) prasugrel and ticagrelor demonstrated to improve angiographic results of primary percutaneous coronary intervention (pPCI) and clinical prognosis, but their onset of action is significantly impaired

The pressure-length relation in normal and ischemic segments was analyzed with use of left ventriculography and simultaneous micromanometry during supine exercise in 9 normal subjects and 12 patients with effort angina. Segmental analysis was done in the right anterior oblique projection using a long axis with three perpendicular, equidistant chords. The apical segment in the 12 patients with coronary artery disease represented the ischemic region. In 5 of the 12 patients with coronary artery disease, the basal segment that showed no exercise-induced deterioration in wall motion was used as an intrapatient control (nonischemic segment).In the 12 patients with coronary artery disease, left ventricular ejection fraction decreased (from 65% to 50%, p < 0.001), end-diastolic pressure increased (from 24 to 40 mm Hg, p < 0.001) and the lowest diastolic filling pressure increased (from 9 to 22 mm Hg, p < 0.001) during exercise-induced ischemia. In normal subjects, ejection fraction increased (from 64% to 70%, p < 0.01) with unchanged end-diastolic pressure, whereas the lowest diastolic filling pressure decreased during exercise (from 9 to 3 mm Hg, p < 0.01). Global left ventricular diastolic pressure-volume curves showed an upward and rightward shift during exercise-induced ischemia. Regional pressure-length curves of both nonischemic (n = 5) and ischemic (n = 12) segments were shifted upward in early diastole, but moved to a higher portion of the rest pressure-length curve without an upward shift during mid- to end-diastole. In contrast, the apical segment in normal subjects showed a downward shift during exercise. Regional stiffness increased during exercise-induced ischemia in the ischemic but not in the nonischemic segment.In conclusion, the global left ventricular diastolic pressure-volume relation shows an upward and rightward shift during exercise-induced ischemia, whereas the regional pressure-length curves of the nonischemic and ischemic segments show an upward shift only during early, but not during late, diastole. This early diastolic upward shift of the regional pressure-length curve is more pronounced in the nonischemic segment. Regional stiffness is increased only in the ischemic segment. Thus, there is a time-dependent upward shift of the regional pressure-length curve during exercise-induced ischemia that is probably due to delayed relaxation in the ischemic segment and increased viscous forces in the nonischemic segment.

Whether exercise-induced vasoconstriction of coronary artery stenoses is modified by the administration of calcium antagonists was examined in 14 patients with classic angina pectoris. In this group the effect of intracoronary diltiazem (2 to 3 mg) on luminal area was evaluated in normal and stenotic segments of epicardial coronary arteries during symptom-limited supine exercise. The luminal area of a normal and a stenotic coronary artery segment was determined by quantitative coronary arteriography with a computer-assisted system. Patients were studied at rest, 6 min after 2 to 3 mg of intracoronary diltiazem, during supine bicycle exercise (96 W) and 5 min after sublingual administration of 1.6 mg nitroglycerin. Heart rate, mean pulmonary and aortic pressure as well as the percent change of both normal and stenotic luminal area were determined.Intracoronary administration of diltiazem was associated with mild dilation of both normal (19%, p < 0.01) and stenotic coronary luminal area (11%, p < 0.05). During subsequent exercise, luminal area of the stenotic vessel segment increased by 23% (p < 0.001) and that of the normal vessel segment by 24% (p < 0.001), whereas in a previously reported control group, luminal area of the stenotic vessel segment decreased by 29% during exercise. After sublingual administration of nitroglycerin, the luminal area of both the normal and the stenotic vessel segment increased further by 19% (p < 0.01) and 22% (p < 0.01), respectively, compared with the values after intracoronary administration of diltiazem.Thus, intracoronary administration of diltiazem prevents exercise-induced vasoconstriction of stenotic coronary arteries, suggesting a direct vasodilating effect on the coronary artery. Diltiazem and nitroglycerin seem to have an additive effect on coronary vasodilation of stenotic vessel segments probably as a result of restoration of endothelial function of the diseased coronary vessel by diltiazem.

Passive diastolic properties of the left ventricle were determined in 10 control subjects and 12 patients with dilated cardiomyopathy. Simultaneous left ventricular angiography and high fidelity pressure measurements were performed in all patients. Left ventricular chamber stiffness was calculated from left ventricular pressure-volume and myocardial stiffness from left ventricular stress-strain relations with use of a viscoelastic model. Patients with dilated cardiomyopathy were classified into two groups according to the diastolic constant of myocardial stiffness (beta). Group 1 consisted of seven patients with a normal constant of myocardial stiffness less than or equal to 9.6 (normal range 2.2 to 9.6) and group 2 of 5 patients with a beta greater than 9.6. Structural abnormalities (percent interstitial fibrosis, fibrous content) in patients with dilated cardiomyopathy were assessed by morphometry from right ventricular endomyocardial biopsies. Heart rate was similar in the three groups. Left ventricular end-diastolic pressure was significantly greater in patients with cardiomyopathy (18 mm Hg in group 1 and 22 mm Hg in group 2) than in the control patients (10 mm Hg). Left ventricular ejection fraction was significantly lower in groups 1 (37%) and 2 (36%) than in the control patients (66%). Left ventricular muscle mass index was significantly increased in both groups with cardiomyopathy. The constant of chamber stiffness (beta*) was slightly although not significantly greater in groups 1 and 2 (0.58 and 0.58, respectively) than in the control group (0.35). The constant of myocardial stiffness beta was normal in group 1 (7.0; control group 6.9, p = NS) but was significantly increased in group 2 (23.5). Interstitial fibrosis was 19% in group 1 and 43% (p less than 0.001) in group 2 (normal less than or equal to 10%). There was an exponential relation between both diastolic constant of myocardial stiffness (beta) and interstitial fibrosis (IF) (r = 0.95; p less than 0.001) and beta and fibrous content divided by end-diastolic volume index (r = 0.93; p less than 0.001). It is concluded that myocardial stiffness can be normal in patients with dilated cardiomyopathy despite severely depressed systolic function. Structural alterations of the myocardium with increased amounts of fibrous tissues are probably responsible for the observed changes in passive elastic properties of the myocardium in patients with dilated cardiomyopathy. The constant of myocardial stiffness (beta) helps to identify patients with severe structural alterations (group 2), representing possibly a more advanced stage of the disease.