Safety of Percutaneous Coronary Intervention Without P2Y12 Inhibitor Pretreatment From a Cohort of Unselected Patients.

OBJECTIVES: Recent studies have challenged systematic pretreatment with a P2Y12 inhibitor before percutaneous coronary intervention (PCI) in elective and non-ST segment elevation myocardial infarction (NSTEMI) patients. The aim of this study was to assess outcomes after performing PCI immediately after coronary angiography with an exclusive "on-the-table" P2Y12 inhibitor loading dose, by evaluating ischemic and bleeding complications in unselected patients. METHODS: Consecutive patients admitted for elective PCI or NSTEMI were included in this two-center, prospective, observational study, and received a P2Y12 inhibitor after coronary angiography when PCI was decided. The primary composite endpoint was first occurrence of cardiovascular death, myocardial infarction, stroke, urgent revascularization, or use of bail-out glycoprotein IIb/IIIa inhibitors at 30 days after PCI. Stent thrombosis and bleeding criteria (Bleeding Academic Research Consortium [BARC]) were evaluated. RESULTS: Among 299 included patients, a total of 188 were admitted for elective PCI and 111 for NSTEMI. The incidence of the primary endpoint was 8.5% (95% confidence interval [CI], 5.7-12.4). No definite stent thrombosis occurred. Three independent predictive factors were associated with the primary endpoint: NSTEMI setting (odds ratio [OR], 5.61; 95% CI, 1.75-17.98), thrombotic coronary lesion (OR, 4.26; 95% CI, 1.45-12.54), and longer procedure duration (OR, 1.06; 95% CI, 1.03-1.09). Clinically relevant bleedings (BARC 2, 3, or 5) occurred in 5.4% of patients. CONCLUSIONS: In an unselected population admitted for elective PCI or NSTEMI in real-world clinical practice, administration of a P2Y12 inhibitor only after coronary angiography is associated with a low rate of ischemic and bleeding events at 30 days.

Hypertensive patients with left ventricular hypertrophy have global left atrial dysfunction and impaired atrio-ventricular coupling.

OBJECTIVE: The aim of this study was to comprehensively investigate left atrial (LA) reservoir, conduit, and booster pump functions, as well as their predictors in patients with primary systemic arterial hypertension (HTN) and left ventricular (LV) hypertrophy. METHODS: Thirty patients with HTN and LV hypertrophy, but no history of atrial arrhythmia or heart failure, were compared with 29 normotensive controls. Speckle-tracking echocardiography of the LA wall was used to measure systolic and diastolic strains and strain rates. Early diastolic velocity of transmitral flow/early diastolic mitral annular motion velocity (E/E')/peak systolic LA strain (S-LAs) was used as an index of LA stiffness. RESULTS: HTN patients had higher LV mass index, impaired LV diastolic function, and higher LA volume index than controls. LA reservoir, conduit, and booster pump functions were significantly lower and LA stiffness was greater. Multiple regression analysis indicated that increased LV mass and LV filling pressures as well as reduced LV strain or E' were predictors for reduced atrial function. CONCLUSION: HTN patients showed a significant impairment of the three components of LA function. These changes were correlated with LV hypertrophy and dysfunction, and presumably related to LA fibrotic changes, underlining the importance of LA-LV coupling. The prognostic value of these new speckle-tracking echocardiography-based LA strain indices needs to be evaluated by future studies.

One-year incidence and clinical impact of bleeding events in patients treated with prasugrel or clopidogrel after ST-segment elevation myocardial infarction.

BACKGROUND: Little information is available on the long-term incidence of bleeding events after ST-segment elevation myocardial infarction (STEMI) with the current antithrombotic strategy. AIMS: To evaluate the effect of bleedings for up to 12months on clinical events and therapeutic compliance in unselected STEMI patients treated with prasugrel or clopidogrel. METHODS: Patients were treated with clopidogrel or prasugrel according to guidelines. The primary endpoint was first occurrence of a bleeding event from hospital discharge to 12months, assessed by the Bleeding Academic Research Consortium (BARC) classification using a dedicated questionnaire. Topography of bleedings, causes of premature cessation and ischaemic events were compared between clopidogrel- and prasugrel-treated patients. RESULTS: A total of 390 patients were enrolled (211 in the prasugrel group, 179 in the clopidogrel group). Elderly, female and low-body weight patients were more likely to receive clopidogrel. At 12months, the incidence of major bleedings (BARC 3) was lower with prasugrel (1% vs 6%; P=0.02), mainly due to fewer transfusions. Elderly age was a risk factor for severe bleeding. Premature treatment cessation was related to ischaemic complications (P=0.03), and occurred more frequently with prasugrel (P=0.001). One-year mortality was very low (1.9 per 100 person-years, 95% confidence interval 0.9-4.0), and was higher in the clopidogrel group (P=0.03). CONCLUSIONS: In this unselected STEMI population, the rate of major bleedings with prasugrel at 12months was low, but nuisance bleedings were frequent and led to more premature cessations than with clopidogrel. Prevention of bleeding complications, even minor, is necessary to prevent disruption of antithrombotic medication.

Exercise response in hypertrophic cardiomyopathy: blunted left ventricular deformational and twisting reserve with altered systolic-diastolic coupling.

BACKGROUND: Abnormal left ventricular (LV) deformational mechanics have been demonstrated in patients with hypertrophic cardiomyopathy (HCM) at rest, but there is a lack of information on their adaptation to exercise. The aim of this study was to assess the adaptability of LV strains and torsional mechanics during exercise in HCM patients. METHODS AND RESULTS: Twenty nonobstructive HCM patients (age, 48.3±12.3 years; 14 men) and 20 control subjects underwent speckle-tracking echocardiographic measurement of longitudinal, radial, and circumferential strains, systolic twist, and diastolic untwisting rate (UTR) at rest and submaximal exercise. HCM patients showed lower resting longitudinal (-15.7±5.0% versus -19.4±2.6%, P<0.001) and radial (38.1±11.3% versus 44.7±14.4%, P<0.05) strains but higher circumferential strain (-21.9±4.0% versus -18.8±2.3%, P<0.05) and twist (15.7±3.6° versus 9.3±2.6°, P<0.0001) than control subjects. Exercise induced an increase in all strains in control subjects but only a moderate increase in longitudinal strain (to -18.4±5.0%), without significant changes in radial and circumferential strains or twist in HCM patients. Exercise peak UTR was lower (-119.0±31.5°/s versus -137.3±41.1°/s) and occurred later (137±18% versus 125±11% systolic time, P<0.05) in HCM than in control subjects. A significant relationship between twist and UTR was obtained in control subjects (ß=-0.0807, P<0.001) but not in HCM patients (ß=-0.0051, P=0.68). CONCLUSIONS: HCM patients had severely limited strain adaptability and no LV twisting reserve at exercise. They had reduced and delayed UTR with reduced systolic-diastolic coupling efficiency by twist-untwist mechanics.

A case of cardiomyopathy induced by inappropriate sinus tachycardia and cured by ivabradine.

We present the case of a 67-year-old woman with cardiomyopathy induced by inappropriate sinus tachycardia (IST) and a particularly high average heart rate. The patient was resistant and/or intolerant to treatment with conventional rate-slowing medications. We used ivabradine--a specific sinus node I(f) current inhibitor--and successfully lowered the heart rate (33 beats per minute mean heart rate decrease). Symptoms, systolic function, and heart rate variability parameters recovered dramatically. No side effect was noted. We suggest that ivabradine--evaluated in trials to treat stable angina--should be considered as a second-line treatment in patients with very symptomatic and refractory IST.

Subclinical cardiac abnormalities in human immunodeficiency virus-infected men receiving antiretroviral therapy.

Although cardiotoxic effects of highly active antiretroviral therapy (HAART) are a growing concern, there is a lack of prospective studies of subclinical involvement of the heart in human immunodeficiency virus (HIV)-infected patients. This study evaluated noninvasively cardiac morphologic characteristics and function in HIV-positive (HIV(+)) men receiving HAART for > or =2 years with no clinical evidence of cardiovascular disease. Echocardiography at rest, including tissue Doppler imaging and exercise testing, were performed in 30 HIV(+) men (age 42.1 +/- 4.7 years, duration of HIV infection 10.4 +/- 4.7 years, duration of HAART 5.3 +/- 2.1 years) and 26 age-matched healthy controls. At rest, HIV(+) patients had similar left ventricular (LV) mass indexed to height(2.7) (40.6 +/- 9.5 vs 37.5 +/- 9.3 g/m; p >0.05), but a higher prevalence of LV diastolic dysfunction (abnormal relaxation or pseudonormal filling pattern in 64% of patients vs 12% of controls; p <0.001). LV systolic function indexes were significantly lower (ejection fraction 60.4 +/- 8.7% vs 66.9 +/- 6.9%; p <0.01, and tissue Doppler imaging peak systolic velocity 11.4 +/- 1.6 vs 13.5 +/- 2.2 cm/s; p <0.001). Pulmonary artery pressure was higher in patients compared with controls (32.1 +/- 5.4 vs 26.1 +/- 6.5 mm Hg; p <0.001). Exercise testing showed decreased exercise tolerance in HIV(+) patients, with no case of myocardial ischemia. In conclusion, subclinical cardiac abnormalities are frequently observed in HIV(+) patients on HAART. The usefulness of systematic noninvasive screening in this population should be considered. GECEM study no. 30: National Agency for AIDS Research (ANRS).

A systems model of training for patients in phase 2 cardiac rehabilitation.

BACKGROUND: The aim of this study was to apply a systems model of training for athletes in patients with coronary artery disease (CAD) undergoing phase 2 cardiac rehabilitation. METHODS: Data from six patients with CAD undergoing 20 conventional training sessions were used to test this model. The method required daily training quantification using heart rate, and regular assessment of real exercise tolerance using a constant-duration test. Convolution of training quantity with real exercise tolerance was provided for every patient model exercise tolerance, by minimizing the residual sum of squares. RESULTS: The results showed that application of the systems model of training to the six patients resulted in a strong fit between real and model exercise tolerances: r(2) = 0.77, 0.79, 0.83, 0.84, 0.85 and 0.92, respectively (P < 0.05). DISCUSSION: Moreover, the systems model admitted for all patients corresponded to one first-order transfer function, which was fitness. This result was in contrast with the systems models reported in athletes and in a patient with CAD undergoing phase 3 cardiac rehabilitation which were found to include two first-order transfer functions: fitness and fatigue, simultaneously. CONCLUSION: The systems model of training of patients with CAD undergoing phase 2 suggested two practical consequences: first, the improvement of exercise tolerance is directly related to training, and consequently second, patients who enter immediately phase 3 training may prevent a decrease in their exercise tolerance.

Applying a systems model of training to a patient with coronary artery disease.

PURPOSE: The aim of the present study was to apply a systems model of training for athletes to a patient with coronary artery disease (CAD) undergoing phase 3 rehabilitation. METHODS: A patient with CAD underwent 14 wk of training during which exercise was quantified using intensity and duration. Real exercise tolerance was assessed twice a week during this period using a constant-load test. The model exercise tolerance was obtained by convolving the quantified training to real exercise tolerance. The model parameters were obtained by fitting the real exercise tolerance to model exercise tolerance by the least square method. These parameters were then used to calculate the time needed after a training impulse to reach maximal tolerance (tg) and then to return to the pretraining level of tolerance (ti). RESULTS: The results showed that: 1) the fit between real and model exercise tolerances was significant (r = 0.73, P < 0.05), and 2) tg and ti were predicted 17 and 120 d posttraining, respectively. CONCLUSIONS: The application of a systems model of training for athletes to a patient with CAD was successful. We were able to predict the maximal exercise tolerance and the duration of increased tolerance subsequent to the training period.