Optimal timing of follow-up cardiac magnetic resonance in patients with uncomplicated acute myocarditis.

BACKGROUND: Cardiac magnetic resonance (CMR) is central in the diagnosis and prognostic stratification of acute myocarditis (AM) but the timing of repeated CMR scans to assess edema resolution and late gadolinium enhancement (LGE) stabilization remain unclear. We assessed edema and LGE evolution over 12 months to identify the optimal timing of repeat CMR evaluation in AM. METHODS AND RESULTS: Thirty-three consecutive patients with AM underwent CMR at clinical presentation (CMR-1), after 3 months (CMR-2) and after 12-months (CMR-3). CMR included assessment of edema and LGE, left ventricular ejection fraction (LVEF) and left ventricular mass index (LVMi). After CMR-3 patients were followed-up every three-months by clinical evaluation, Holter-monitoring, and echocardiography. All patients had edema and LGE at CMR-1. At CMR-2 edema-positive segments (0.42 ± 0.34 vs. 3.18 ± 2.33, p < 0.005), LGE (4.98 ± 4.56 vs. 9.60 ± 8.58 g, and 4.22 ± 3.97% vs 7.50 ± 5.61%) and LVMi (69.82 ± 11.83 vs 76.06 ± 13.13 g/m2) (all p < 0.0001) significantly reduced, while LVEF (63.12 ± 5.47% vs.61.15 ± 6.87% p < 0.05) significantly improved, compared to CMR-1. At CMR-2 edema persisted in 7 patients (21%) but resolved at CMR-3 with no further changes of LVMi, LVEF and LGE. During follow-up (85 ± 15 months), 5 (15%) patients showed persistent ventricular arrhythmias. Univariate predictors of arrhythmic persistence were LGE extension at CMR-2 and CMR-3 (both p < 0.05), but not at CMR-1 (p = 0.07). CONCLUSIONS: Most patients with uncomplicated AM show edema resolution with LGE stabilization after 3 months. Further CMR evaluations should be limited to patients with persisting edema at this time. LGE extent measured after edema resolution is associated with persistent ventricular arrhythmias.

Beyond Sarcomeric Hypertrophic Cardiomyopathy: How to Diagnose and Manage Phenocopies.

PURPOSE OF REVIEW: We describe the most common phenocopies of hypertrophic cardiomyopathy, their pathogenesis, and clinical presentation highlighting similarities and differences. We also suggest a step-by-step diagnostic work-up that can guide in differential diagnosis and management. RECENT FINDINGS: In the last years, a wider application of genetic testing and the advances in cardiac imaging have significantly changed the diagnostic approach to HCM phenocopies. Different prognosis and management, with an increasing availability of disease-specific therapies, make differential diagnosis mandatory. The HCM phenotype can be the cardiac manifestation of different inherited and acquired disorders presenting different etiology, prognosis, and treatment. Differential diagnosis requires a cardiomyopathic mindset allowing to recognize red flags throughout the diagnostic work-up starting from clinical and family history and ending with advanced imaging and genetic testing. Different prognosis and management, with an increasing availability of disease-specific therapies make differential diagnosis mandatory.

Abnormal coronary reserve and left ventricular wall motion during cold pressor test in patients with previous left ventricular ballooning syndrome.

AIMS: To investigate whether and how cold pressor test (CPT) could affect myocardial perfusion and left ventricular (LV) function in patients with previous LV ballooning syndrome (LVBS). METHODS AND RESULTS: Cold pressor test (3 min hand immersion in ice-water) was performed in 17 women with previous LVBS and in 7 age- and risk factor-matched women with chest pain and normal coronary arteries. At baseline and peak CPT, global and regional LV function, and myocardial perfusion were quantitatively assessed by real-time three-dimensional echocardiography (RT3DE) and myocardial contrast (SonoVue, Bracco) 2D echocardiography (MCE), respectively (Philips iE33 machine, X3-1 and S5-1 probes). Data were analysed off-line (QLab 6.0 software). Peripheral venous catecholamines were assayed by high performance liquid chromatography with electrochemical detection. Cold pressor test induced similar haemodynamic changes and catecholamine increase in controls and LVBS patients. Left ventricular ejection fraction decreased and transient new mid-ventricular and apical motion abnormalities developed in LVBS patients only (quantitative RT3D analysis), without corresponding perfusion defects (MCE). At peak CPT, coronary blood flow and velocity increased (quantitative MCE analysis) in control subjects only. CONCLUSION: Cold pressor test induced LV wall motion abnormalities unmatched to regional coronary flow reduction in LVBS patients only. The reduced coronary reserve in response to CPT suggests microvascular dysfunction in LVBS patients.

Primary percutaneous coronary intervention in comatose survivors of cardiac arrest with ST-elevation acute myocardial infarction: a single-center experience in Florence.

OBJECTIVE: Primary percutaneous coronary intervention is currently known as the most effective reperfusion strategy in patients with ST-elevation myocardial infarction. There are no formal recommendations from the American Heart Association/American College of Cardiology and European Society of Cardiology guidelines regarding the treatment of comatose patients with signs of ST-elevation myocardial infarction after reestablishment of spontaneous circulation. METHODS: We assessed prognosis in 31 consecutive comatose ST-elevation myocardial infarction patients admitted to our intensive cardiac care unit after early percutaneous coronary intervention from 1 January 2005 to 30 June 2006. RESULTS: During intensive cardiac care unit stay, eight patients died (8/23, 34.7%). In comparison between patients who died and those who survived, the former were older (P = 0.049), showed a higher incidence of chronic obstructive pulmonary disease and had a shorter intensive cardiac care unit length of stay (P = 0.001). No differences were detectable in the two subgroups regarding angiographic characteristics. The incidence of thrombolysis in myocardial infarction grade 3 postpercutaneous coronary intervention was higher in patients who survived (P = 0.0437). Patients who died showed higher latency times, both symptoms-to-basic life support and symptoms-emergency-team (P = 0.0171 and 0.0116, respectively). Patients who survived showed a higher ejection fraction than those who died, as well as lower values of peak troponin I, leukocytes and glycemia (P = 0.01, 0.001 and 0.05, respectively). CONCLUSION: According to our data, comatose survivors undoubtedly present a high-risk subgroup of ST-elevation myocardial infarction population in which percutaneous coronary intervention shows a procedural efficacy similar to conscious ST-elevation myocardial infarction patients and whose prognosis seems to be related both to infarct size and to neurological status. Further studies need to be performed in this high-risk subgroup investigating the effects of mild hypothermia (mainly on the neurological outcome) as well as the feasibility, safety and outcome of assistance device.