Vai ai contenuti. | Spostati sulla navigazione | Spostati sulla ricerca | Vai al menu | Contatti | Accessibilità

| Crea un account

Cacciavillani, Luisa (2008) Magnetic resonance imaging of acute myocardial infarction: an insight into pathophysiology. [Tesi di dottorato]

Full text disponibile come:

[img]
Anteprima
Documento PDF
3932Kb

Abstract (inglese)

.Recently cardiac magnetic resonance (CMR) has been proposed as a comprehensive tool for AMI evaluation, since it provides data about regional myocardial wall motion, viability, perfusion and direct visualization of myocardial necrosis. In this respect, the aims of this study performed in AMI patients treated with primary angioplasty (PCI), were:
1.to clarify the impact of reperfusion time on pregression of myocardial damage;
2.to assess the predictive value of CMR features on ventricular post-AMI remodelling;
3.to investigate, with contrast-CMR, the pathological basis of the persistence of ST-segment elevation after AMI;
4.to evaluate the effects of current therapy on CMR detection of necrosis and microvascular injury;
5.to evaluate the correlation between angiographic indexes of myocardial perfusion after primary PCI, and anatomical features on CMR and in particular the correlation between the staining phenomenon and the presence of severe microvascular damage (SMD);
6.to investigate the possibility to detect intramyocardial hemorrhage after AMI by T2-weighted image on CMR, to establish its contribution to the delayed hypoenhanced core, traditionally referred only to microvascular obstruction. We also aimed to correlate radiolagical findings of myocardial hemorrhage with hystological features ex vivo in two died patients.
In AMI patients with impaired coronary perfusion undergoing PCI, the risk of transmural necrosis (TN) and SMD seems to increase with the duration of the ischemic time. Also, the amount of TN results as a major determinant of LV remodeling and function, with significant additional predictive value to infarct size and SMD. The evaluation of effects of current therapy with Abciximab demonstrated that SMD seems related to TN without any influence of antiplatelet therapy. In addition, presence of SMD seems the most powerful determinant of persistent ST-segment elevation on ECG. In our experience the angiographic assessment of lack of myocardial perfusion correlates with microvascular damage and extent of infarct

Abstract (italiano)

I pazienti inclusi nello studio dal dicembre 2005 all’ottobre 2008 sono stati 300. Per ogni paziente sono stati raccolti i dati di MRI insieme a dati clinici, ecocardiografici, elettrocardiografici ed agiografici.
1.Il primo studio, condotto su una serie di pazienti selezionati in base ad un flusso TIMI preprocedurale inferiore a 3, ha dimostrato che la durata dell’ischemia miocardica rappresenta il maggior determinante della transmuralità di necrosi e della presenza di danno microvascolare. In particolare nei 64 pazienti analizzati, con un tempo medio di ischemia di 190±110 min; l’analisi multivariata ha confermato che il ritardo nel trattamento riperfusivo era correlato sia con la transmuralità di necrosi (odds ratio per 30 min, 1.37, p = 0.032), sia con la presenza di severo danno microvascolare (odds ratio per 30 min, 1.21; p = 0.021), entrambi valutati mediate MRI.
2.Nei primi 76 pazienti è stata inoltre valutata l’influenza della transmuralità di necrosi, dell’infarct size e della presenza di zone di ostruzione microvascolare sul rimodellamento ventricolare: analizzando tutti questi parametri è emerso in questa prima serie di pazienti che la transmuralità di necrosi è il maggior determinante del remodeling; l’infarct size e l’ostruzione microvascolare alla MRI presentavano un valore predittivo aggiunto rispetto alla transmuralità stessa. In questa esperienza preliminare i volumi ventricolari sono stati valutati mediante follow-up ecocardiografico con una media di 6±1 mesi dall’evento acuto. In particolare all’analisi univariata la necrosi transmurale, la severa ostruzione microvascolare, l’infarct size ed I livelli di troponina I (valori di picco) risultavano direttamente correlati con il rimodellamento ventricolare ed inversamente associati alla frazione d’eiezione al follow-up (p <0.001). All’analisi mutlivariata, solo la necrosi transmurale ed i livelli di troponina I emergevano come predittori indipendenti di rimodellamento ventricolare. Inoltre la necrosi transmurale si dimostrava un più potente predittore di rimodellamento, sia in termini di volumi ventricolari (R2 = 0.19), sia di funzione sistolica (R2 = 0.16).
3.Raccogliendo i dati clinici dei pazienti anche durante il follow-up è stato possibile anche raccogliere i dati inerenti gli eventi maggiori, in particolare il decesso per cause cardiache: due dei soggetti seguiti nel follow-up sono stati oggetto di una analisi comparativa delle immagini alla MRI nel post-AMI con i reperti autoptici ed istologici, nonché con i dati derivati dalle MRI eseguite ex-vivo in questi stessi pazienti. Dall’analisi delle immagini T1 e T2 pesate è emerso che le aree ipointense identificate come core ipointenso nell’ambito dell’area di necrosi ed attribuite fino ad allora solo a fenomeni di no-reflow intravascolare, in realtà corrispondevano a zone di vera emorragia intramiocardica. In particolare le aree a basso segnale osservate nelle sequenze T2 ex-vivo, correlavano fortemente con l’emorragia quantificata all’istologia (R = 0.93, p = 0.0007).
4.Un analisi successiva si è proposta di valutare il peso delle nuove terapie antiaggreganti sulla genesi di tale fenomeno. I nostri dati indicano come la presenza di aree ipointense dopo gadolinio siano più legate alla presenza di necrosi transmurale piuttosto che all’impiego di farmaci antiaggreganti per via infusiva come l’Abciximab. In particolare suddividendo i pazienti in due gruppi in base all’impiego di Abciximab, i pazienti in cui tale strategia terapeutica è stata messa in atto presentavano una transmuralità di necrosi pari a 3.03±2.8 segmenti rispetto ai 3.09±2.9 (p=0,9) del gruppo controllo; analogamente la presenza di severa ostruzione microvascolare non si associava ad una terapia specifica impiegata (1.05±1.5 versus 1.06±1.8 segmenti). All’analisi multivariata la severa ostruzione microvascolare risultava correlata esclusivamente con la transmuralità di necrosi (O.R. 1.5; p<0,001) e l’età (O.R. 1.1; p=0.02), ma non alla somministrazione di Abciximab.
5.Un successivo sviluppo è stato quindi quello di valutare in vivo l’incidenza, a partire dalle osservazioni desunte dai due casi autoptici, dell’infarto emorragico definito come stria mesoventricolare ipointensa in T2 ed in T1 (all’interno dell’hyperenhancement tardivo della cicatrice post-infartuale): nella nostra casisistica, analizzando solo i casi di AMI transmurale, è emerso che circa il 37% degli IMA presentava fenomeni di emorragia intramiocardica.
6.Infine abbiamo confrontato, indipendentemente dall’estensione della necrosi, i tradizionali parametri angiografici di mancata perfusione miocardica dopo PTCA ( flusso TIMI e Mycardial Blush Grade MBG) con la presenza alla MRI di aree di no- reflow (identificate come aree di hypoenhancment tardivo). E’ emersa una significativa correlazione (p< 0.001) tra scarsa o assente riperfusione all’angiografia e presenza alla MRI di zone di ostruzione del microcircolo. Inoltre all’interno dei pazienti con MBG. pari a 0 è stato possibile identificare i casi con staining angiografico, indicativo di “spandimento” di mezzo di contrasto nel muscolo cardiaco: tale reperto risultava strettamente associato, anche da un punto di vista topografico, con la presenza di hypoenhancement tardivo, e quindi con segni MRI di emorragia intramiocardica.
Conclusioni Il nostro lavoro ha permesso di identificare mediante uno studio prospettico, consecutivo, tutti i dati inerenti la caratterizzazione tissutale mediante MRI del miocardio dopo AMI. Successivi studi di follow-up già in corso in una casistica così numerosa forniranno il reale significato prognostico di queste osservazioni.


Statistiche Download - Aggiungi a RefWorks
Tipo di EPrint:Tesi di dottorato
Relatore:Basso, Cristina
Dottorato (corsi e scuole):Ciclo 21 > Scuole per il 21simo ciclo > SCIENZE MEDICHE, CLINICHE E SPERIMENTALI > SCIENZE CARDIOVASCOLARI
Data di deposito della tesi:02 Febbraio 2009
Anno di Pubblicazione:2008
Parole chiave (italiano / inglese):infarto miocardico, risonanza magnetica cardiaca
Settori scientifico-disciplinari MIUR:Area 06 - Scienze mediche > MED/11 Malattie dell'apparato cardiovascolare
Struttura di riferimento:Dipartimenti > Dipartimento di Scienze Medico Diagnostiche e Terapie Speciali
Codice ID:1987
Depositato il:02 Feb 2009
Simple Metadata
Full Metadata
EndNote Format

Bibliografia

I riferimenti della bibliografia possono essere cercati con Cerca la citazione di AIRE, copiando il titolo dell'articolo (o del libro) e la rivista (se presente) nei campi appositi di "Cerca la Citazione di AIRE".
Le url contenute in alcuni riferimenti sono raggiungibili cliccando sul link alla fine della citazione (Vai!) e tramite Google (Ricerca con Google). Il risultato dipende dalla formattazione della citazione.

Phibbs B, Marcus F, Marriott HJC, et al. Q-wave versus non-Q-wave myocardial infarction: A meaningless distinction. J Am Coll Cardiol 1999, 33:576–582. Cerca con Google

Braunwald E, Antman EM, Beasley JW, et al. ACC-AHA Guidelines for the management of patients with unstable angina. J Am Coll Cardiol 2000; 36: 970. Cerca con Google

Boersma E, Mercado N, Poldermans D, et al. Acute myocardial infarction. Lancet 2003; 361: 847. Cerca con Google

Braunwald E, Antman EM, Beasley JW, et al: ACC-AHA 2002 Guideline update for the management of patients with unstable angina and non-ST segment elevation myocardial infarction-summary article. J Am Coll Cardiol 2002; 40:1366. Cerca con Google

Zipes, Libby, Bonow, Brounwald: Braunwald’s Heart Disease, A Text Book of Cardiovascular Medicine, 7° edition, Elsevier Saunders, 2005. Cerca con Google

Reimer KA, Lowe JE, Rasmussen MM, et al. The wavefront phenomenon of ischemic cell death. 1. Myocardial infarct size vs duration of coronary occlusion in dogs. Circulation 1977; 56:788–94. Cerca con Google

Reimer KA, Jennings RB. The ‘‘wavefront phenomenon’’ of myocardial ischemic cell death: II. Transmural progression of necrosis within the framework of ischemic bed size (myocardium at risk) and collateral flow. Lab Invest 1979; 40:633–44. Cerca con Google

DeWood MA, Spores J, Notske RN, et al. Prevalence of total coronary artery occlusion during the early hours of transmural myocardial infarction. N Engl J Med 1980; 303: 897–902. Cerca con Google

Fujita M, Nakae I, Kihara Y, et al. Determinants of collateral development in patients with acute myocardial infarction. Clin Cardiol 1999; 22: 595–599. Cerca con Google

Davies MJ. The pathophysiology of acute coronary syndromes. Heart 2000; 83:361–6. Cerca con Google

Vargas SO, Sampson BA, Schoen FJ. Pathologic detection of early myocardial infarction: A critical review of the evolution and usefulness of modern techniques. Mod Pathol 1999; 12: 635–645. Cerca con Google

Braunwald E, Kloner RA. Myocardial reperfusion: a double-edged sword? J Clin Invest 1985; 76:1713–9. 101 Cerca con Google

Maxwell SRJ, Lip GYH. Reperfusion injury: a review of the pathophysiology,clinical manifestations and therapeutic options. Int J Cardiol 1997; 58: 95–117. Cerca con Google

Kloner R. Does reperfusion injury exist in humans? J Am Coll Cardiol 1993; 21: 537. Cerca con Google

Basso C, Thiene G. The pathophysiology of myocardial reperfusion: a pathologist’s perspective. Heart 2006; 92: 1559–1562. Cerca con Google

Ambrosio G, Tritto I. Reperfusion injury: experimental evidence and clinicalimplications. Am Heart J 1999; 138: S69–75. Cerca con Google

Baroldi G. Different types of myocardial necrosis in coronary heart disease: a pathophysiologic review of their functional significance. Am Heart J 1975; 89: 742–52. Cerca con Google

Buja LM. Myocardial ischemia and reperfusion injury. Cardiovasc Pathol 2005; 14:170–5. Cerca con Google

Kloner RA, Ganote CE, Jennings RB. The ‘‘no-reflow’’ phenomenon after temporary coronary occlusion in the dog. Clin Invest 1974; 54:1496–1508. Cerca con Google

Kloner RA, Ellis SG, Lange R, et al: Studies of experimental coronary artery reperfusion: Effects on infarct size, myocardial function, biochemistry, ultrastructure and microvascular damage. Circulation 1983; 68: 15–18. Cerca con Google

Reffelmann T, Kloner RA. Microvascular alterations after temporary coronary artery occlusion: The no-reflow phenomenon. J Cardiovasc Pharmacol Ther 2004; 9: 163–172. Cerca con Google

Dignan RJ, Kadletz M, Dyke CM, Lutz HA, Yeh T Jr, Wechsler AS. Microvascular dysfunction after myocardial ischemia. J Thorac Cardiovasc Surg 1995; 109: 892–897. Cerca con Google

Carlson RE, Aisen AM, Buda AJ. Effect of reduction in myocardial edema on myocardial blood flow and ventricular function after coronary reperfusion. Am J Physiol 1992; 262: H641–H648. Cerca con Google

Manciet LH, Poole DC, McDonagh PF, Copeland JG, Mathieu-Costello O. Microvascular compression during myocardial ischemia: Mechanistic basis for no-reflow phenomenon. Am J Physiol 1994; 266: H1541–H1550. Cerca con Google

Reffelmann T, Kloner RA. Microvascular reperfusion injury: Rapid expansion of anatomic no-reflow during reperfusion in the rabbit. Am J Physiol Heart Circ Physiol 2002; 283: H1099–H1107. 102 Cerca con Google

Reffelmann T, Kloner RA. The no-reflow phenomenon: A basic mechanism of myocardial ischemia and reperfusion. Basic Res Cardiol 2006; 101: 359–372. Cerca con Google

Stone GW, Webb J, Cox DA, et al for the Enhanced Myocardial Efficacy and Recovery by Aspiration of Liberated Debris (EMERALD) Investigators. Distal microcirculatory protection during percutaneous coronary intervention inacute ST-segment elevation myocardial infarction: a randomized controlled trial. JAMA 2005; 293: 1063–72. Cerca con Google

Basso C, Bacchion F, Ramondo A, et al. A postmortem investigation of distal coronary microembolization in acute coronary syndromes. Lab Invest 2006; 86(suppl 1): 46A. Cerca con Google

Xu Y, Huo Y, Toufektsian MC et al. Activated platelets contribute importantly to myocardial reperfusion injury. Am J Phisiol Heart Circ Physiol 2006; 290: H692-H699. Cerca con Google

Heindl B, Zahler S, Welsch U, Becker BF. Disparate effects of adhesion and degranulation of platelets on myocardial and coronary function in postischaemic hearts. Cardiovasc Res 1998; 38: 383-394. Cerca con Google

Niccoli G, Giubilato S, Russo E et al. Plasma levels tromboxane A2 on admission are associated with no-reflow after primary percutaneous coronary intervention. Eur Heart J 2008; 29: 1843-1850. Cerca con Google

Okamura A, Ito H, Iwakura K, Kawano S, Inoue K, Yamamoto K, Ogihara T, Fujii K. Usefulness of a new grading system based on coronary flow velocity pattern in predicting outcome in patients with acute myocardial infarction having percutaneous coronary intervention. Am J Cardiol 2005; 96: 927–932. Cerca con Google

Iwakura K, Ito H, Nishikawa N, Hiraoka K, Sugimoto K, Higashino Y, Masuyama T, Hori M, Fujii K, Minamino T. Early temporal changes in coronary flow velocity patterns in patients with acute myocardial infarction demonstrating the ‘‘no-reflow’’ phenomenon. Am J Cardiol 1999; 84: 415–419. Cerca con Google

Agostini F, Iannone MA, Mazzucco R, Cionini F, Baccaglioni N, Lettieri C et al.. Coronary flow velocity pattern assessed by transthoracic Doppler echocardiography predicts adverse clinical events and myocardial recovery after successful primary angioplasty. J Cardiovasc Med (Hagerstown) 2006; 7: 753–760. Cerca con Google

Albert TSE, Kim RJ, Judd RM. Assessment of no-reflow regions using cardiac MRI. Basic Res Cardiol 2006; 101: 383–390. 103 Cerca con Google

Gibson CM, Murphy SA, Rizzo JM, et al. Relationship between TIMI frame count and clinical outcomes after trombolytic administration. Thrombolysis In Myocardial Infarction (TIMI) Study Group. Circulation 1990; 99: 1945-50. Cerca con Google

van’t Hof AWJ, Liem A, Suryapranata H, Hoorntje JCA, de Boer MJ, Zijlstra F. Angiographic assessment of myocardial reperfusion in patients treated with primary angioplasty for acute myocardial infarction. Myocardial Blush Grade, Circulation 1998; 97: 2302-6. Cerca con Google

Fishbein MC, Rit J, Lando U, et al. The relationship of vascular injury and myocardial hemorrhage to necrosis after reperfusion. Circulation 1980; 62:1274–9. Cerca con Google

Garcia-Dorado D, Theroux P, Solares J, et al. Determinants of hemorrhagic infarcts. Histologic observations from experiments involving coronary occlusion, coronary reperfusion, and reocclusion. Am J Pathol 1990; 137: 301–11. Cerca con Google

Tennant R, Wiggers CJ: The effect of coronary occlusion on myocardial contractions. Am J Physiol 1935; 112: 351. Cerca con Google

Heyndrickx GR, Millard RW, McRitchie RJ, et al: Regional myocardial functional and electrophysiological alterations after brief coronary artery occlusion in conscious dogs. J Clin Invest 1975; 56: 978–985. Cerca con Google

Kloner RA, Bolli R, Marban E, et al: Medical and cellular implications of stunning, hibernation, and preconditioning: An NHLBI workshop. Circulation 1998; 97:1848–1867. Cerca con Google

Bolli R, Marban E: Molecular and cellular mechanisms of myocardial stunning. Physiol Rev 1999; 79: 609–634. Cerca con Google

Bolli R: Basic and clinical aspects of myocardial stunning. Prog Cardiovasc Dis 1998; 40:477–516. Cerca con Google

Majidi M, Kosinski AS, Al-Khatib SM. Reperfusion ventricular arrhythmia 'bursts' in TIMI 3 flow restoration with primary angioplasty for anterior ST-elevation myocardial infarction: a more precise definition of reperfusion arrhythmias. Europace 2008 Aug; 10(8):988-97. Cerca con Google

Vera Z, Pride HP, Zipes DP. Reperfusion arrhythmias: role of early afterdepolarizations studied by monophasic action potential recordings in the intact canine heart during autonomically denervated and stimulated states. J Cardiovasc Electrophysiol 1995 Jul; 6(7):532-43. 104 Cerca con Google

Gibbons RJ , Valeti US, Araoz PA, Jaffe AS. The quantification of infarct size. J Am Coll Cardiol 2004; 44: 1533– 42. Cerca con Google

Wu E, Judd RM, Vargas JD, Klocke FJ, Bonow RO and Kim RJ. Visualisation of presence, location, and transmural extent of healed Q-wave and non–Q-wave myocardial infarction. Lancet 2001; 357: 21–28. Cerca con Google

Choi KM, Kim RJ, Gubernikoff G, Vargas JD, Parker M and Judd RM. Transmural extent of acute myocardial infarction predicts long-term improvement in contractile function. Circulation 2001; 104: 1101–1107. Cerca con Google

Petersen SE, Horstick G, Voigtlander T et al. Diagnostic value of routine clinical parameters in acute myocardial infarction: a comparison to delayed contrast enhanced magnetic resonance imaging: Delayed enhancement and routine clinical parameters after myocardial infarction. Int J Cardiovasc Imaging 2003; 19: 409–416. Cerca con Google

Gerber BL, Garot J, Bluemke DA, Wu KC and Lima JA. Accuracy of contrast-enhanced magnetic resonance imaging in predicting improvement of regional myocardial function in patients after acute myocardial infarction. Circulation 2002; 106: 1083–1089. Cerca con Google

Kim RJ, Wu E, Rafael A et al. The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med 2000; 343: 1445–1453. Cerca con Google

Wu KC, Zerhouni EA, Judd RM, et al. Prognostic significance of microvascular obstruction by magnetic resonance imaging in patients with acute myocardial infarction. Circulation 1998; 97: 765-72. Cerca con Google

Thygesen K, Alpert JS, White HD. Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial InfarctionUniversal definition of myocardial infarction. Eur Heart J. 2007 Oct; 28(20): 2525-38. Cerca con Google

Kim RJ, Albert TS, Wible JH et al. Performance of delayed-enhancement magnetic resonance imaging with with gadoversetamide contrast for the detection and assessment of myocardial infarction: an international, multicenter, double-blinded, randomized trial. Circulation 2008; 117: 629 –37. Cerca con Google

Lombardi M, Bartolozzi C. Risonanza Magnetica del cuore e dei vasi, Ed. Springer 2006. Cerca con Google

Selvanayagam JB, Robson MD, Francis JM & Neubauer S. Cardiac CT, PET and MR. Chapter 2. Ed. Blackwell Futura 2006. 105 Cerca con Google

Simonetti OP, Kim RJ, Fieno DS et al. An improved MR imaging technique for the visualization of myocardial infarction. Radiology 2001; 218: 215–223. Cerca con Google

Bucciarelli-Ducci C, Wu E, Lee DC, Holly TA, Klocke FJ, Bonow RO. Contrast-enhanced cardiac magnetic resonance in the evaluation of myocardial infarction and myocardial viability in patients with ischemic heart disease. Curr Probl Cardiol. 2006 Feb; 31(2): 128-68. Cerca con Google

Grobner T. Gadolinium-a specific trigger for the development of nephrogenic fibrosing dermopathy and nephrogenic systemic fibrosis? Nephrol Dial Transplant 2006; 21: 1104–8. Cerca con Google

Singh M, Davenport A, Clatworthy I, et al. A follow-up of four cases of nephrogenic systemic fibrosis: is gadolinium the specific trigger? Br J Dermatol 2008; 158: 1358–62. Cerca con Google

Swaminathan S, High WA, Ranville J, et al. Cardiac and vascular metal deposition with high mortality in nephrogenic systemic fibrosis. Kidney Int 2008; 73: 1413– 8. Cerca con Google

Schroeder JA, Weingart C, Coras B, et al. Ultrastructural evidence of dermal gadolinium deposits in a patient with nephrogenic systemic fibrosis and end-stage renal disease. Clin J Am Soc Nephrol 2008; 3: 968–75. Cerca con Google

Thomsen HS. ESUR guideline: gadolinium-based contrast media and nephrogenic systemic fibrosis. Eur Radiol 2007; 17: 2692–6. Cerca con Google

Kaandorp TA, Lamb HJ, Bax JJ, van der Wall EE, de Roos A. Magnetic resonance imaging of coronary arteries, the ischemic cascade, and the myocardial infarction. Am J Cardiol 2005; 149: 200-8. Cerca con Google

Gould KL, Lipscomb K. Effects of coronary stenosis on the coronary flow reserve and resistance. Am J Cardiol 1974; 34: 48-55. Cerca con Google

Chiu CW, So NM, Lam WW et al. Combined first-pass perfusion and viability study at MR imaging in patients with non-ST segment elevation acute coronary syndromes: feasibility study. Radiology 2003; 226: 717-22. Cerca con Google

Rogers WJ Jr, Kramer CM, Geskin G, et al. Early contrast-enhanced MRI predicts late functional recovery after reperfused myocardial infarction. Circulation. 1999; 99: 744-50. Cerca con Google

Rochitte CE, Lima JA, Bluemke DA, et al. Magnitude and time course of microvascular obstruction and tissue injury after myocardial infarction. Circulation 1998; 98: 1006-14. 106 Cerca con Google

Gerber BL, Rochitte CE, Melin JA, McVeigh ER, Bluemke DA, Wu KC et al. Microvascular obstruction and left ventricular remodeling early after acute myocardial infarction. Circulation 2000; 101(23): 2734-41. Cerca con Google

Hombach V, Grebe O, Merkle N, et al. Sequelae of acute myocardial infarction regarding cardiac structure and function and their prognostic significance as assessed by magnetic resonance imaging. Eur Heart J. 2005; 26: 549-57. Cerca con Google

Lund GK, Stork A, Saeed M, et al. Acute Myocardial Infarction: Evaluation with First-Pass Enhancement and Delayed Enhancement MR Imaging Compared with 201Tl SPECT Imaging. Radiology 2004; 232: 49-57. Cerca con Google

Abdel-Aty H, Zagrosek A, Schulz-Menger J, et al. Delayed enhancement and T2-weighted cardiovascular magnetic resonance imaging differentiate acute from chronic myocardial infarction. Circulation 2004; 109: 2411–6. Cerca con Google

Natanzon A, Aletras AH, Hsu L, Arai AE. Determininig canine myocardial area at risk with manganese-enhanced MR imaging. Radiology 2005; 236: 859-866. Cerca con Google

Friedrich MG. There is more than shape and function size J Am Coll Cardiol 2008; 51: 1581-7. Cerca con Google

van den Bos EJ, Baks T, Moelker AD,et al. Magnetic resonance imaging of haemorrhage within reperfused myocardial infarcts: possible interference with iron oxide-labelled cell tracking? Eur Heart J 2006; 27: 1620-1626. Cerca con Google

Rehwald W, Fieno DS, Chen EL, et al. Myocardial magnetic resonance imaging contrast agent concentration after reversible and irreversible ischemic injury. Circulation 2002; 105: 224-9. Cerca con Google

Kim RJ, Choi KM, Judd RM.Assessment of myocardial viability by contrast enhancement. In: Higgins CB, De Roos A, editors. Cardiovascular MRI and MRA. Philadelphia, PA: Lippincott Williams & Wilkins, 2003: p. 209-37 Cerca con Google

Brasch RC, Weinmann HJ, Wesbey GE. Contrast-enhanced NMR imaging: animal studies using gadolinium-DTPA complex. AJR Am J Roentgenol 1984;142: 625-30. Cerca con Google

Saeed M, Lund G, Wendland MF, et al. Magnetic resonance characterization of the peri-infarction zone of reperfused myocardial infarction with necrosis-specific and extracellular nonspecific contrast media. Circulation 2001; 103: 871-6. 107 Cerca con Google

Kim RJ, Chen EL, Lima JAC, et al. Myocardial Gd-DTPA kinetics determine MRI contrast enhancement and reflect the extent and severity of myocardial injury after acute reperfused infarction. Circulation 1996; 94: 3318-26. Cerca con Google

Oshinski JN, Yang Z, Jones JR, et al. Imaging time after Gd-DTPA injection is critical in using delayed enhancement to determine infarct size accurately with magnetic resonance imaging. Circulation 2001; 104: 2838-42. Cerca con Google

Ingkanisorn WP, Rhoads KL, Aletras AH, Kellman P, Arai AE. Gadolinium delayed enhancement cardiovascular magnetic resonance correlates with clinical measures of myocardial infarction.J Am Coll Cardiol 2004; 43: 2253-9. Cerca con Google

Hillenbrand HB, Kim RJ, Parker MA, et al. Early assessment of myocardial salvage by contrast-enhanced magnetic resonance imaging. Circulation 2000; 102: 1678-83. Cerca con Google

Selvanayagam JB, Kardos A, Francis JM, et al. Value of delayed-enhancement cardiovascular magnetic resonance imaging in predicting myocardial viability after surgical revascularization. Circulation 2004; 110: 1535-41. Cerca con Google

Judd RM, Lugo-Olivieri CH, Arai M, et al. Physiological basis of myocardial contrast enhancement in fast magnetic resonance images of a 2-day-old reperfused canine infarcts. Circulation 1995; 92: 1902-10. Cerca con Google

Schlegel JU. Demonstration of blood vessels and lymphatics with a fluorescent dye in ultraviolet light. Anat Rec 1949; 105: 433-53. Cerca con Google

Rochitte CE, Kim RJ, Hillebrand HB, et al. Microvascular integrity and the time course of myocardial sodium accumulation after acute infarction. Circ Res 2000; 87: 648-55. Cerca con Google

Ito H, Maruyama A, Iwakura K, et al. Clinical implication of the ‘no-reflow’ phenomenon: a predictor of complications and left ventricular remodeling in reperfused anterior wall myocardial infarction. Circulation 1996; 93: 223-8. Cerca con Google

Wu E, Tejedor P, Lee DC, et al. No reflow detected by delayed contrast enhancment predicts remodeling following an ST-segment myocardial infarction. Circulation 2004; 110: III-444 [abstract]. Cerca con Google

Azevedo CF, Amado LC, Kraitchman DL et al. The effect of intraaortic balloon counterpulsation on left ventricular functional recovery early after acute myocardial inarction: a randomized experimental magnetic resonance imaging study. Eur Heart J 2005; 26 (12): 1235-41. 108 Cerca con Google

Amado LC, Kraitchman DL, Gerber BL, et al. Reduction of “no-reflow” phenomenon by intra-aortic balloon conuterpulsation in a randomized magnetic resonance imaging experimental study. J Am Coll Cardiol 2004; 43: 1291-8. Cerca con Google

Rentrop KP, Cohen M, Blanke H, Phillips RA. Changes in the collateral channel filling immediately after controlled coronary artery occlusion by an angioplasty balloon in human subject. J Am Coll Cardiol 1985; 5: 587–592. Cerca con Google

Cohen M, Rentrop KP. Limitation of myocardial ischemia by collateral circulation during sudden controlled coronary artery occlusion in human subjects: a prospective study. Circulation. 1986; 74(3): 469-76. Cerca con Google

C. M. Gibson and A. Schomig Coronary and Myocardial Angiography: Angiographic Assessment of Both Epicardial and Myocardial Perfusion Circulation 2004; 109(25): 3096–3105. Cerca con Google

Henriques JPS, Zijlstra F, van’t Hof AWJ, Menko-jan de Boer, Jan-Henk E Dambrink, Gosselink M, et al. Angiographic assessment of reperfusion in acute myocardial infarction by myocardial blush grade. Circulation 2003; 107:2115-19. Cerca con Google

Little WC, Rogers EW. Angiographic evidence of hemorrhagic myocardial infarction after intracoronary thrombolysis with streptokinase. Am J Cardiol 1983 Mar 1; 51(5): 906-8. Cerca con Google

Tarantini G, Ramondo A, Napodano M et al. Myocardial perfusion grade and survival after percutaneous transluminal coronary angioplasty in patients with cardiogenic shock. Am J Cardiol 2004; 93: 1081–1085. Cerca con Google

Cerqueira MD, Weissman NJ, Dilsizian V, et al. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart: a statement for healthcare professional from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association. Circulation 2002; 105: 539-42. Cerca con Google

Lima JA, Judd RM, Bazille A, et al. Regional heterogeneity of human myocardial infarcts demonstrated by contrast-enhanced MRI. Circulation 1995; 92: 1117–25. Cerca con Google

Beek AM, Kuhl HP, Bondarenko O, et al. Delayed contrast-enhanced magnetic resonance imaging for the prediction of regional functional improvement after acute myocardial infarction. J Am Coll Cardiol 2003; 42: 895–901. Cerca con Google

Tibrewala AV, Asch F, Shah S, Fuisz A, Lindsay J Jr. Association of size of myocardial scar and persistence of ST-segment elevation after healing of anterior wall myocardial infarction. Am J Cardiol 2007; 99: 1106-8. Cerca con Google

Mollet NR, Dymarkowski S, Volders W, Wathiong J, Herbots L, Rademakers FE et al. Visualization of ventricular thrombi with contrast-enhanced magnetic resonance imaging in patients with ischemic heart disease. Circulation. 2002; 106(23): 2873-6. Cerca con Google

Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommitee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr 1989; 2: 358-67. Cerca con Google

Konen E, Merchant N, Gutierrez C, Provost Y, Mickleborough L, Paul NS, et al. True versus false left ventricular aneurysm: differentiation with MR imaging-initial experience. Radiology 2005; 236: 65-75. Cerca con Google

Reimer KA, Heide RSV, Richard VJ. Reperfusion in acute myocardial infarction: effect of timing and modulating factors in experimental models. Am J Cardiol 1993; 72: 13G–21G. Cerca con Google

Reffelmann T, Hale SL, Li G, Kloner RA. Relationship between no reflow and infarct size as influenced by the duration of ischemia and reperfusion. Am J Physiol 2002; 282: H766–72. Cerca con Google

De Luca G, Suryapranata H, Ottervanger JP, Antman EM. Time delay to treatment and mortality in primary angioplasty for acute myocardial infarction: every minute of delay count. Circulation 2004; 109:1223–5 Cerca con Google

Rizzello V, Poldermans D, Boersma E, Biagini E, Schinkel AFL, Krenning B et al. Opposite patterns of left ventricular remodeling after coronary revascularization in patients with ischemic cardiomyopathy. Role of myocardial viability. Circulation 2004; 110: 2383–2388. Cerca con Google

Bologense L, Cerisano G, Buonamici P, Santini A, Santoro GM, Antoniucci D et al. Influence of infarct-zone viabilità on left ventricular remodeling after acute myocardial infarction. Circulation 1997; 96: 3353-3359. Cerca con Google

Nijland F, Kamp O, Verhorst PMJ, WG de Voogt, Bosh HG, Visser CA. Myocardial viability: impact on left ventricular dilatation after acute myocardial infarction. Heart 2002; 87: 17-22. Cerca con Google

Bolognese L, Neskovic AN, Parodi G, Cerisano G, Buonamici P, Santoro GM et al. Left ventricular remodeling after primary coronary angioplasty. Patterns of left ventricular dilation and long-term prognostic inplications. Circulation 2002; 106: 2351-57. Cerca con Google

Morton J. Kern Patterns of Left Ventricular Dilatation With an Opened Artery After Acute Myocardial Infarction Circulation. Circulation 2002;106: 2294-2295. Cerca con Google

Mills RM Jr, Young E, Gorlin R, Lesch M. Natural history of ST-segment elevation after acute myocardial infarction. Am J Cardiol 1975; 35: 609-614. Cerca con Google

Chon K, Dymnicka S, Forlini FJ Jr. Use of electrocardiogram as an aid in screening for left ventricular aneurysm. J Electrocardiol 1976; 9: 53-58. Cerca con Google

Arvan S, Varat MA. Persistent ST-segment elevation and left ventricular wall abnormalities: a 2-dimensional echocardiographic study. Am J Cardiol 1984; 53: 1542-46. Cerca con Google

Herman MV, Heinle RA, Klein MD, Gorlin R. Localized disorders in myocardial contraction. Asynergy and its role in congestive heart failure. N Engl J Med 1967; 277: 222-232. Cerca con Google

Bar FW, Brugada P, Dassen WR, van der Werf T, Wellens HJ. Prognostic value of Q waves, R/S ratio, loss of R wave voltage, ST-T segment abnormalities, electrical axis, low voltage and notching: correlation of electrocardiogram and left ventriculogram. J Am Coll Cardiol 1984; 4:17-27. Cerca con Google

Lindsay J Jr, Dewey RC, Talesnick BS, Nolan NG. Relation of ST-segment elevation after healing of acute myocardial infarction to the presence of left ventricular aneurysm. Am J Cardiol 1984; 54: 84-6. Cerca con Google

Bhatnagar SK. Observations of the relationship between left ventricular aneurysm and ST segment elevation in patients with a first acute anterior Q wave myocardial infarction. Eur Heart J 1994; 15: 1500-1504. Cerca con Google

Tibrewala AV, Asch F, Shah S, Fuisz A, Lindsay J Jr. Association of size of myocardial scar and persistence of ST-segment elevation after healing of anterior wall myocardial infarction. Am J Cardiol 2007; 99: 1106-8. Cerca con Google

Li RA, Reppo M, Miki T, Seino S, Marbàn E. Molecular basis of electrocardiographic ST-segment elevation. Circ Res 2000; 87: 837-39. Cerca con Google

Link MS, Wang PJ, VanderBrink BA, Avelar E, Pandian NG, Maron BJ, et al. Selective activation of the KATP channel is a mechanism by which sudden death is produced by low-energy chest-wall impact (commotio cordis). Circulation 1999; 100: 413-18. Cerca con Google

Gussak I, Wright RS, Kopecky SL, Hammil SC. Exercise-induced ST segment elevation in Q wave leads in postinfarction patients: defining its meaning and utility in today’s practice. Cardiology 2000; 93: 205-209. Cerca con Google

De Luca G, Suryapranata H, Stone G, et al. Abciximab as adjunctive therapy to reperfusion in acute ST-segment elevation myocardial infarction. JAMA 2005; 293: 1759–1765. Cerca con Google

Godicke J, Flather M, Noc M, et al. Early versus periprocedural administration of abciximab for primary angioplasy: a pooled analysis of 6 studies. Am Heart J 2005; 150: 1015e11–1015e17 Cerca con Google

Maioli M, Bellandi F, Leoncini M, Toso A, Dabizi RP. Randomized early versus late abciximab in acute myocardial infarction treated with primary coronary intervention (RELAx-AMI trial). J Am Coll Cardiol 2007; 49: 1517–1524 Cerca con Google

Rakowski T, Zalewski J, Legutko J, et al. Early abciximab administration before primary percutaneous coronary intervention improves infarct-related artery patency and left ventricular function in high risk patients with anterior wall myocardial infarction: a randomized study. Am Heart J 2007; 153: 360–365. Cerca con Google

Reimer KA, Jennings RB, Cobb FR, et al. Animal models for protection ischemic myocardium: results of the NHLBI Cooperative Study. Comparison of unconscious and conscious dog models. Circ Res 1985; 56: 651– 665 Cerca con Google

De Luca G, Ernst N, Zijlstra F, et al. Preprocedural TIMI flow and mortality in patients with acute myocardial infarction treated by primary angioplasty. J Am Coll Cardiol 2004; 43: 1363–1367. Cerca con Google

Fernandez-Avilés F, Alonso JJ, Pena G, et al. Primary optimal percutaneous coronary intervention versus facilitated intervention (tenecteplase plus stenting) in patients with ST-elevated acute myocardial infarction (GRACIA-2). Eur Heart J 2007, E-pub ahead of print. Cerca con Google

Ross AM, Coyne KS, Reiner JS, et al. A randomized trial comparing primary angioplasty with a strategy of short-acting thrombolysis and immediate planned rescue angioplasty in acute myocardial infarction: the PACT trial. Cerca con Google

PACT investigators. Plasminogen- activator Angioplasty Compatibility Trial. J Am Coll Cardiol 1999; 34: 1954– 1962. Cerca con Google

Petronio AS, Rovai D, Musumeci G, et al. Effects of abciximab on microvascular integrity and left ventricular functional recovery in patients with acute infarction treated by primary coronary angioplasty. Eur Heart J 2003; 24: 67–76. Cerca con Google

Sciagrà R, Parodi G, Pupi A, et al. Gated SPECT evaluation of outcome after abciximab- supported primary infarct artery stenting for acute myocardial infarction: the scintigraphic data of the abciximab and carbostent evaluation (ACE) randomized trial. J Nucl Med 2005; 46: 722–27. Cerca con Google

Montalescot G, Barragan P, Wittenberg O, et al. Platelet glycoprotein IIb/IIIa inhibition with coronary stenting for acute myocardial infarction. N Engl J Med 2001; 344: 1895–1903. Cerca con Google

Neumann FJ, Blasini R, Schmitt C, et al. Effect of glycoprotein IIb/IIIa receptor blockade on recovery of coronary flow and left ventricular function after the placement of coronary-artery stents in acute myocardial infarction. Circulation 1998; 98: 2695–2701. Cerca con Google

Reffelman T, Kloner RA. The ‘no-reflow’ phenomenon: basic science and clinical correlates.Heart 2002; 87: 162–168. Cerca con Google

Costantini CO, Stone GW, Mehran R, et al: Frequency, correlates, and clinical implications of myocardial perfusion after primary angioplasty and stenting, with and without glycoprotein IIb/IIIa inhibition, in acute myocardial infarction. J Am Coll Cardiol 2004; 44: 305–312. Cerca con Google

Iliceto S, Marangelli V, Marchese A, et al. Myocardial contrast echocardiography in acute myocardial infarction: pathophysiological background and clinical applications. Eur Heart J 1996; 17: 344-353. Cerca con Google

Dong J, Ndrepepa G, Schmitt C, Mehilli J, Schmieder S, Schwaiger M, et al. Early resolution of ST-segment elevation correlates with myocardial salvage assessed by Tc-99m sestamibi scintigraphy in patients with acute myocardial infarction after mechanical or thromolytic reperfusion therapy. Circulation 2002; 105: 2946-2949. Cerca con Google

Appelbaum E, Ajay J Kirtane Alica Clark, et al. Association of TIMI Myocardial Perfusion Grade and ST-segment resolution with cardiovascular magnetic resonance measures of microvascular obstruction and infarct size Cerca con Google

following ST-segment elevation myocardial infarction. J Thromb Thrombolysis. 2008 Feb 2. Epub ahead of print Cerca con Google

Porto I, Burzotta F, Brancati M, Trani C, et al. Realtionship of myocardial blush grade to microvascular perfusion and myocardial infarct size after primary or rescue percutaneous coronary intervention. Am J Cardiol 2007; 99:1671-1673. Cerca con Google

Thulborn KR, Biochemical basis of the MRI appearance of cerebral hemorrhage. In:Edelman RR, Hesslink JR, Zlatkin MB, Crues JV, eds. Clinical Magnetic Resonance Imaging. 3rd ed. Philadelphia, PA: Saunders, 2006:174-186. Cerca con Google

Iwakura K, Ito H, Kawano S, et al. Predictive factors for development of the no-reflow phenomenon in patients with reperfused anterior wall acute myocardial infarction. J Am Coll Cardiol 2001; 38: 472-478. Cerca con Google

Galiuto L, Garramone B, Scarà A, Rebuzzi AG, Crea F, La Torre G, et al AMICI Investigators. The extent of microvascular damage during myocardial contrast echocardiography is superior to other known indexes of post-infarct reperfusion in predicting left ventricular remodeling: results of the multicenter AMICI study. J Am Coll Cardiol. 2008 Feb 5;51(5):552-9. Cerca con Google

Shishido T, Beppu S, Matsuda H, Miyatake K. Progression of intramural hemorrhage in the reperfused area: an experimental study assessed by myocardial contrast echocardiography. Circulation. 1993; 88(suppl I):I-402. Cerca con Google

de Roos A, van Rossum AC, van der Wall E, Postema S, et al. Reperfused and nonreperfused myocardial infarction: diagnostic potential of Gd-DTPA-enhanced MR imaging. Radiology 1989; 172: 717-720. Cerca con Google

Ewout J. van den Bos, Baks T, Moelker AD, Kerver W, van geuns RJ, van der Giessen WJ et al. Magnetic resonance imaging of haemorrhage within reperfused myocardial infarcts: possible interference with iron oxide-labelled cell tracking? European Heart Journal 2006; 27: 1620-1626. Cerca con Google

Asanuma T, Tanabe K, Ochiai K, Yoshitomi H, Nakamura K, Murakami Y, et al. Relationship between progressive microvascular damage and intramyocardial hemorrhage in patients with reperfused anterior myocardial infarction. Circulation 1997; 96: 448-53. Cerca con Google

Ochiai K, Shimada T, Murami Y, Ishibashi Y, Sano K, Kitamura J, et al. Hemorrhagic myocardial infarction after coronary reperfusion detected in vivo by magnetic resonance imaging in humans: prevalence and clinical implications. J cardiovasc Magn Resonan 1999; 1: 247-256. Cerca con Google

Becker RC, Charlesworth A, Wilcox RG. Cardiac rupture associated with thrombolytic therapy: impact of time to treatment in the Late Assessment of Thrombolytic Efficacy (LATE) study.J Am Coll Cardiol 1995; 25: 1063-1068. Cerca con Google

Factor SM, Robinson TF, Dominitz R, Cho SH. Alterations of the myocardial skeletal framework in acute myocardial infarction with and without ventricular rupture. A preliminary report. Am J Cardiovascular Pathol 1987; 1: 91-7. Cerca con Google

Charney RH, Takahashi S, Zhao M, Sonnenblick EH, Eng C. Collagen loss in the stunned myocardium Circulation 1992; 85: 2123-34. Cerca con Google

Peuhkurinen KJ, Risteli L, Melkko JT ey al.Thrombolytic therapy with streptokinase stimulates collagen breakdown Circulation 1991; 83: 1969-75. Cerca con Google

Maggioni AP et al., GISSI-2. Age-Related Increase in Mortality among Patients with First Myocardial Infarctions Treated with Thrombolysis NEJM 1993; 329: 1442-48. Cerca con Google

Honan MB, Harrell FE Jr, Reimer KA, Califf RM, Mark DB, Pryor DB, and MA Hlatky Cardiac rupture, mortality and the timing of thrombolytic therapy: a meta-analysis J Am Coll Cardiol 1990; 16: 359-367. Cerca con Google

Download statistics

Solo per lo Staff dell Archivio: Modifica questo record