Cardiomiopatia restrittiva
Le cardiomiopatie restrittive (CMPR) sono un gruppo eterogeneo di malattie del muscolo cardiaco accomunate dal fatto che il ventricolo sinistro (o, più di rado, entrambi i ventricoli) presenta(no) un pattern di riempimento diastolico di tipo restrittivo con volume diastolico generalmente ridotto, pareti incostantemente aumentate di spessore e funzione sistolica normale o modicamente ridotta. L’espressione “pattern restrittivo” indica che durante la diastole vi è un ostacolo al riempimento del ventricolo, il quale non riesce ad accogliere il sangue perché le sue pareti sono rigide e poco distensibili. Di conseguenza, la pressione diastolica ventricolare aumenta e tale incremento si riflette a monte per cui si manifesta ipertensione anche nell’atrio, nelle vene tributarie dell’atrio, nei capillari, ecc.. Il termine (CMPR) deve essere riservata esclusivamente a quelle patologie cardiache il cui pattern restrittivo costituisce l’elemento caratterizzante il quadro fisiopatologico.
Esistono forme primitive e secondarie di CMPR. Tra le prime vanno incluse la cosiddetta CMPR idiopatica (talvolta familiare con trasmissione di tipo autosomico dominante), la sindrome di Loeffler e la fibrosi endomiocardica. Le forme secondarie comprendono le CMPR infiltrative (sarcoidosi amiloidosi ecc..) e quelle di accumulo (emocromatosi, ecc..) ognuna di queste condizioni presenta specifici quadri istopatologici. Tuttavia, in linea generale, il reperto macroscopico è quello di un cuore con atri marcatamente dilatati e spesso sede di trombi, mentre i ventricoli appaiono grossolanamente normali.
Sintomatologia
Nella maggior parte dei casi, le prime manifestazioni cliniche sono rappresentate da sintomi e segni di scompenso cardiaco quali:
ridotta tolleranza allo sforzo
dispnea parossistica notturna e ortopnea
edemi declivi
ascite.
La comparsa di fibrillazione atriale è un evento frequente nei soggetti con forme idiopatiche o secondarie ad amiloidosi; circa un terzo dei pazienti può presentare episodi tromboembolic Nonostante la relativamente bassa frequenza di aritmie minacciose (blocco atrio-ventricolare di terzo grado o tachicardia ventricolare), la morte improvvisa rappresenta comunque un evento possibile. L’esame obiettivo consente di rilevare valori di pressione arteriosa normali o ridotti con tendenza all’ ipotensione ortostatica in una significativa percentuale di pazienti. Spesso è presente tachicardia a riposo.
Dati di laboratorio e strumentali
In generale, nelle CMPR idiopatiche non sono presenti significative alterazioni dei parametri ematochimici. Il riscontro di indici di flogosi alterati e di ipereosinofilia orienta verso un’ endocardite di Loeffler. Nelle forme di amiloidosi possono essere presenti diversi alterazioni quali:
. anemia
. leucocitosi
. elevazione della velocità di eritrosedimentazione e
della proteina C-reattiva
. ipofibrinogenemia
. iposideremia
. monoclonalità all’ immunoelettroforesi proteica
. segni di compromissione della funzione renale ed epatica.
La radiografia del torace può mettere in evidenza un aumento delle dimensioni dell’ombra cardiaca, segni di congestione interstiziale o alveolare e versamento pleurico.
L’elettrocardiogramma è l’indagine diagnostica cardine,
mediante la quale è possibile evidenziare un ventricolo sinistro
non ingrandito, con spessori parietali normali o solo lievemente aumentati e con funzione di pompa normale o quasi.
L’ispessimento e l’aspetto granulare delle pareti del ventricolo sinistro in particolare del setto interventricolare è caratteristico delle forme amiloidosiche. Il veicolo destro può presentarsi dilatato, specie nei casi con ipertensione polmonare. E’
pressoché costantemente documentabile una dilatazione
biatriale. Le valvole atrio-ventricolari appaiono frequentemente ispessite, e spesso si associa un rigurgito mitralico e tricuspidale.
L‘ecocardiogramma transesofageo può essere utile per ricercare in modo più accurato l’eventuale presenza di trombi endocavitari. Sebbene l’integrazione dei dati ottenibili dalla valutazione clinica e dagli esami strumentali non invasivi consenta nella maggior parte dei casi di correre correttamente la diagnosi, il cateterismo cardiaco e la biopsia endomiocardica conserva un ruolo importante nello studio della CMPR.
Cenni di Terapia
In generale, la terapia farmacologica delle CMPR si avvale del diuretico per una terapia sintomatica della congestione secondaria allo scompenso cardiaco diastolico. Il dosaggio dei diuretici deve essere stabilito con cautela, per evitare una sindrome da bassa portata conseguente eccessiva riduzione del precarico. Nei pazienti affetti da amiloidosi cardiaca devono essere evitati la digitale e calcio- antagonisti in quanto questi farmaci possono causare fenomeni tossici anche con dosaggi generalmente ritenuti terapeutici. In caso di fibrillazione atriale, è necessario tentare di ristabilire il ritmo sinusale perché l’assenza del contributo atriale al riempimento ventricolare comporta un sostanziale peggioramento della disfunzione diastolica.
A questo scopo, sono indicati sia la cardioversione elettrica che quella farmacologica
mediante l’impiego di agenti antiaritmici, in particolare l’amiodarone.
In caso di difetti di conduzione atrio-ventricolare di grado avanzato può rendersi necessario l’impianto di un pacemaker.
Iltrattamento anticoagulante orale è indicato nei pazienti con rischio tromboembolico, in particolare in quelli con riscontro ecocardiografico di trombi endocavitari, marcata dilatazione atriale, episodi ricorrenti di fibrillazione atriale parossistica o fibrillazione atriale cronica. Non esiste al momento la possibilità di migliorare l’evoluzione delle forme idiopatiche con trattamenti farmacologici specifici e nelle fasi avanzate, il trapianto cardiaco rappresenta l’unica valida opzione terapeutica.
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