http://www.cnr.it/ontology/cnr/individuo/prodotto/ID323259

Myocardial contractility in the stress echo lab: from pathophysiological toy to clinical tool (Articolo in rivista)

Type

Prodotto della ricerca (Classe)
Articolo in rivista (Classe)

Label

Myocardial contractility in the stress echo lab: from pathophysiological toy to clinical tool (Articolo in rivista) (literal)

Anno

2013-01-01T00:00:00+01:00 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi

10.1186/1476-7120-11-41 (literal)

Alternative label

Bombardini T, Zoppè M, Ciampi Q, Cortigiani L, Agricola E, Salvadori S, Loni T, Pratali L, Picano E (2013)
Myocardial contractility in the stress echo lab: from pathophysiological toy to clinical tool
in Cardiovascular ultrasound; Biomed Central Ltd., London (Regno Unito)
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

Bombardini T, Zoppè M, Ciampi Q, Cortigiani L, Agricola E, Salvadori S, Loni T, Pratali L, Picano E (literal)

Rivista

Cardiovascular ultrasound (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

CNR, Institute of Clinical Physiology, Pisa, Italy, Division of Cardiology, Fatebenefratelli Hospital, Benevento, Italy, Division of Cardiology, Campo di Marte Hospital, Lucca, Italy. Division of Non-Invasive Cardiology, San Raffaele University Hospital, Milan, Italy. (literal)

Titolo

Myocardial contractility in the stress echo lab: from pathophysiological toy to clinical tool (literal)

Abstract

Up-regulation of Ca2+ entry through Ca2+ channels by high rates of beating is involved in the frequency-dependent regulation of contractility: this process is crucial in adaptation to exercise and stress and is universally known as force-frequency relation (FFR). Disturbances in calcium handling play a central role in the disturbed contractile function in myocardial failure. Measurements of twitch tension in isolated left-ventricular strips from explanted cardiomyopathic hearts compared with non-failing hearts show flat or biphasic FFR, while it is up-sloping in normal hearts. Starting in 2003 we introduced the FFR measurement in the stress echo lab using the end-systolic pressure (ESP)/End-systolic volume index (ESVi) ratio (the Suga index) at increasing heart rates. We studied a total of 2,031 patients reported in peer-reviewed journals: 483 during exercise, 34 with pacing, 850 with dobutamine and 664 during dipyridamole stress echo. We demonstrated the feasibility of FFR in the stress echo lab, the clinical usefulness of FFR for diagnosing latent contractile dysfunction in apparently normal hearts, and residual contractile reserve in dilated idiopathic and ischemic cardiomyopathy. In 400 patients with left ventricular dysfunction (ejection fraction 30 ± 9%) with negative stress echocardiography results, event-free survival was higher (p < 0.001) in patients with ?ESPVR (the difference between peak and rest end-systolic pressure-volume ratio, ESPVR) >= 0.4 mmHg/mL/m2. The prognostic stratification of patients was better with FFR, beyond the standard LV ejection fraction evaluation, also in the particular settings of severe mitral regurgitation or diabetics without stress-induced ischemia. In the particular setting of selection of heart transplant donors, the stress echo FFR was able to correctly select 34 marginal donor hearts efficiently transplanted in emergency recipients. Starting in 2007, we introduced an operatorindependent cutaneous sensor to monitor the FFR: the force is quantified as the sensed pre-ejection myocardial vibration amplitude. We demonstrated that the sensor-derived force changes at increasing heart rates are highly related with both max dP/dt in animal models, and with the stress echo FFR in 220 humans, opening a new window for pervasive cardiac heart failure monitoring in telemedicine systems. (literal)

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