BackgroundQ waves and negative T waves are common electrocardiographic (ECG) abnormalities in patients with Hypertrophic Cardiomyopathy (HCM). Several studies correlated ECG findings with presence and extent of fibrosis and hypertrophy; however, their significance remains incompletely clarified. Our study aimed to explain the mechanism behind Q and negative T waves by comparing their positions on a 12-lead ECG with phenotypes observed at Late Gadolinium Enhancement (LGE) Cardiac Magnetic Resonance (CMR).Methods12-lead ECG and LGE-CMR were performed in 88 consecutive patients with HCM (42 SD 16 years, 65 males). Using Delta Thickness ratio (DT ratio), and “global” and “parietal” LGE at CMR, the extent and distribution of myocardial hypertrophy and fibrosis were studied in correlation with ECG abnormalities.ResultsQ waves in different leads were not associated with “parietal” LGE score. Lateral Q waves correlated with an increased DT ratio Inferior Septum/Lateral wall (p = 0.01). A similar correlation between inferior Q waves and an increased DT Ratio Anterior wall/Inferior wall was of borderline statistical significance (p = 0.06). As expected, ECG signs of LV hypertrophy related to a raised Left Ventricular Mass Index (LVMI) (p < 0.0001) and mean wall thickness (p = 0.01). Depolarization disturbances, including negative T waves in lateral (p = 0.044) and anterior (p = 0.031) leads correlated with “parietal” LGE scores while QT dispersion (p = 0.0001) was associated with “global” LGE score.ConclusionIn HCM patients, Q waves are generated by asymmetric hypertrophy rather than by myocardial fibrosis, while negative T waves result from local LGE distribution at CMR.

Baroreflex sensitivity (BRS) measured several days after myocardial infarction (MI) is a powerful predictor of cardiovascular mortality. No information is available on BRS in the early hours of MI. The possibility to reliably assess BRS in the acute phase of MI and its clinical correlates were evaluated in 45 patients treated with primary percutaneous coronary intervention (pPCI). BRS (sequence method) was assessed 1, 3, 6, and 12 h after PCI. ST resolution (STRes) was considered present if ST had decreased ≥70 % 3 h after PCI. BRS was 10.7 ± 6.2 1 h after PCI; at 12 h it was 15.4 ± 5.2 and 8.4 ± 4.8 ms/mmHg in patients with and without STRes, respectively (p < 0.001). STRes was an independent predictor of 12 h BRS (p = 0.005) and of 1-12 h BRS difference (p = 0.002). BRS can be reliably assessed in the first hours of MI; it shows a rapid recovery in patients with STRes and a significant depression in patients without STres.

A 57–years–old man with no previous cardiovascular history presented with fever, hypotension, dyspnoea at rest and chest pain. The electrocardiogram showed sinus tachycardia, PR–segment depression and diffuse concave–upwards ST–segment elevation. Elevated C–reactive protein and low pro–BNP level were found at lab tests, procalcitonin and troponin were negative. Chest X–ray showed bilateral pleural effusion. Transthoracic echocardiogram (TTE) revealed mild–to–moderate serofibrinous pericardial effusion with initial diastolic collapse of right chambers, suggesting cardiac pre–tamponade. Because of the exiguity of liquid component, pericardiocentesis was not performed, patient was stabilized by fluid–challenge with hypertonic solution. Ibuprofen and colchicine were started. Left thoracentesis was performed removing one liter of fluid overall compatible with transudate. Cytological and microbiological examinations were negative. Despite of initial clinical improvement, the patient showed kidney failure and worsening of lung failure; perianal abscess was detected causing sepsis and requiring surgical drainage and antibiotic therapy with vancomycin and piperacillin/tazobactam. Culture exams were negative. After ibuprofen replacement with indomethacin a repeated TTE showed reduced pericardial effusion, but also respiratory variation in ventricular filling with signs of interventricular dependence. Cardiac magnetic resonance showed thickening and high signal intensity of pericardial layers on T2 weighted imaging and ventricular septal shift on free–breathing cine sequences, suggesting effusive–constrictive pericarditis. Left and right cardiac catheterization demonstrated ventricular “dip and plateau” pattern and ventricular discordance. Considering the lack of clinical improvement on medical therapy, off–bypass pericardiectomy was performed. Incomplete adhesion between the two pericardial layers and thick gelatinous material were found. After surgery patient experienced rapid clinical improvement; cardiac index increased from 1.5 to 3.5 L/min/m2. Effusive–constrictive pericarditis is a rare and dreaded complication of acute pericarditis. Surgery, when appropriated, is crucial for prognosis. In our case initial response to anti–inflammatory therapy with reduced pericardial effusion unmasked constrictive physiology in an effusive–constrictive pericarditis. Clinical management was complicated by sepsis which could have played a role in constriction developing.