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Tesi etd-11252019-214916


Tipo di tesi
Tesi di specializzazione (5 anni)
Autore
CORSI, ELISABETTA
URN
etd-11252019-214916
Titolo
Comparison between echocardiography and cardiac magnetic resonance for differential diagnosis of left ventricular hypertrophy
Dipartimento
PATOLOGIA CHIRURGICA, MEDICA, MOLECOLARE E DELL'AREA CRITICA
Corso di studi
MALATTIE DELL'APPARATO CARDIOVASCOLARE
Relatori
relatore Prof. Pedrinelli, Roberto
relatore Dott. Aquaro, Giovanni Donato
Parole chiave
  • cardiac amyloidosis
  • cardiac magnetic resonance
  • echocardiography
  • hypertrophic cardiomyopathy
  • Left ventricular hypertrophy
Data inizio appello
18/12/2019
Consultabilità
Non consultabile
Data di rilascio
18/12/2089
Riassunto
Background: Left ventricular hypertrophy (LVH) may be due to different causes, ranging from benign secondary forms (athlete’s heart) to severe prognosis cardiomyopathies (i.e. cardiac amyloidosis). Early and accurate differential diagnosis is important to proper patient management. LVH may be detected by echocardiography and ECG signs of hypertrophy or other abnormalities often associated to hypertrophic phenotypes. Cardiac magnetic resonance (CMR) is often used to confirm the initial diagnostic suspicion. To the best of our knowledge, there are no study specifically designed to evaluate the final impact of CMR in changing or confirming the initial diagnostic echocardiographic suspicion.
Aim: to evaluate the clinical prognostic correlates of CMR in patients with echocardiographic or ECG suspicion of LVH (or cardiomyopathies with hypertrophic phenotype).
Methods: We enrolled 275 pts with echocardiographic evidence of LVH and 25 pts with ECG signs of LVH or abnormalities often associated with hypertrophic phenotypes (with apparently normal echo). Using current guidelines, the initial echocardiographic diagnostic suspicion was: hypertrophic cardiomyopathy (HCM) in 44% of pts; cardiac amyloidosis in 14%; hypertensive LVH in 16%; aortic stenosis in 1.4%; athlete’s heart in 0.3%; undetermined LVH in 16.3%; absence of LVH in 8%. CMR changed the diagnosis in 42.3% cases: the diagnosis of HCM increased from 44% to 71% of pts; hypertensive and undetermined LVH decreased significantly (respectively to 4% and 5%). CMR also identified HCM in 17 out of 25 patients with apparently normal echo but with ECG abnormalities. Finally, the change in diagnostic suspicion was associated to reclassification of risk of patients: Kaplan-Meier curves demonstrated that HCM and cardiac amyloidosis had worst prognosis than undetermined or hypertensive LVH.
Conclusions: CMR changed the echocardiographic suspicion in almost half of patients with LVH. In the subgroup of patients with abnormal ECG suggesting LVH or cardiomyopathies with LVH phenotype and apparently normal echo, CMR identified LVH (particularly HCM) in 80% of patients. This study highlights the indication of CMR in patients with ECG or echocardiographic suspicion of LVH.
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