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Objective: Patients with Takotsubo syndrome (TTS) present an acute microvascular dysfunction that leads to an impaired myocardial perfusion and, in more severe forms, an impaired epicardial flow. However, clinical relevance of a delayed coronary flow, the coronary slow flow (CSF), has never been investigated. We studied the prognostic value of CSF occurring in the acute phase of TTS., Methods: This cohort study prospectively evaluated patients with a diagnosis of TTS. CSF was defined as angiographically non-obstructive coronary arteries with thrombolysis in myocardial infarction-2 flow. The incidence of overall mortality and major adverse cardiovascular events (MACEs), defined as the composite of TTS recurrence, cardiac rehospitalisation, cerebrovascular events and mortality, was assessed at follow-up., Results: We enrolled 101 patients (mean age 71.0±11.1 years, 86 (85.1%) female); CSF occurred in 18 (17.8%) patients. At admission, patients with CSF presented more frequently with Killip class III/IV, moderate-to-severe left ventricle systolic dysfunction and right ventricle dysfunction. During the index admission, patients with CSF had a higher rate of intrahospital complications (12 (66.7%) vs 28 (33.7%), p=0.01). At long-term follow-up, patients with CSF had a significantly higher occurrence of overall mortality (9 (50%) vs 19 (22.9%), p=0.011), mainly due to non-cardiac causes (89.3%), and a higher rate of MACE (10 (55.5%) vs 27 (32.5%), p=0.06). At multivariable Cox regression, CSF was independently associated with death from any causes., Conclusions: Patients with TTS presenting with CSF have a worse clinical presentation with a higher rate of intrahospital complications and a poor long-term clinical outcome., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.)

Patent foramen ovale (PFO) is a known cause of cryptogenic stroke and, when associated with a condition of thrombophilia, its closure has been shown to reduce the recurrence of cerebral embolic events. Here we present a case of a young man, with a history of previous recurrent cerebral ischaemic episodes, that developed an inferior acute myocardial infarction (AMI) with angiographic evidence of thrombotic occlusion of the right coronary artery (RCA). Thrombus aspiration followed by balloon angioplasty was performed and, after 24 h of glycoprotein IIb/IIIa inhibitor infusion, thrombus was no longer evident at coronary angiography. Screening for thrombophilia revealed heterozygosis for prothrombin G20210A polymorphism. At transoesophageal echocardiography (TOE), a large PFO with right-to-left atrial shunt was present. Given the history of multiple thrombotic clinical events and the associated state of thrombophilia, transcatheter PFO closure was successfully performed. At 12 months of follow-up the patient was completely asymptomatic.

Background: In the thrombolytic era, persistence of ST-segment elevation was considered a marker of left ventricular (LV) aneurysm. ST-segment elevation may still be found persistently raised after successful primary percutaneous coronary intervention (PCI). Echocardiographic correlates of this finding, however, are still poorly known., Methods and Results: 82 consecutive patients with first ST-segment elevation myocardial infarction and successful PCI were divided into patients with persistent ST-segment elevation at discharge (sum of ST >4 mm) (n = 33) and those without persistent ST-segment elevation (n = 49). Conventional and myocardial contrast echocardiography were performed at discharge and at 6 months. At discharge, LV aneurysm was more common in patients with persistent ST elevation (27% vs 8%, p<0.005). Similarly, the wall motion score index was higher (2.5 vs 2.0, p<0.005) and microvascular damage larger (2.3 vs 1.8, p<0.005) in patients with persistent ST-segment elevation. At 6 months' follow-up, LV volumes were similar in the two groups., Conclusions: After primary PCI, persistent ST-segment elevation is associated with LV aneurysm formation in 30% of cases, it is not associated with significantly larger LV dilatation but with larger microvascular damage and dysfunctioning risk area.

Background: Recent studies have shown that microvascular dysfunction after myocardial infarction is a dynamic phenomenon., Aims: To evaluate the implications of dynamic changes in microvascular dysfunction on contractile recovery and left ventricular remodelling, and to identify the ideal timing of assessment of such microvascular dysfunction., Methods and Results: In 39 patients with a first myocardial infarction who underwent successful percutaneous coronary intervention, microvascular dysfunction was studied by myocardial contrast echocardiography (MCE) at 24 h, 1 week and 3 months after the procedure. Real-time MCE was performed by contrast pulse sequencing and intravenous Sonovue. 14 patients exhibited left ventricular remodelling at 3 months (>20% increase in left ventricular end-diastolic volume, group B), whereas 25 did not (group A). Microvascular dysfunction was similar in the two groups at 24 h and improved in group A only, being significantly better than that of group B at 1 week (p<0.05) and 3 months (p<0.005). Improvement in microvascular dysfunction was not associated with improvement in wall motion in the same segments. With multivariate analysis including all echocardiographic variables, microvascular dysfunction at 1 week was found to be the only independent predictor of left ventricular remodelling (p<0.01). With a cut-off value of 1.4, 1-week microvascular dysfunction predicts left ventricular remodelling with sensitivity and specificity of 73%., Conclusions: Improvement in microvascular dysfunction occurs early after myocardial infarction, although it is not associated with a parallel improvement in wall motion but is beneficial in preventing left ventricular remodelling. Accordingly, 1-week microvascular dysfunction is a powerful and independent predictor of left ventricular remodelling.

Objective: To test the hypothesis that impaired coronary and myocardial blood flow are linked with increased myocyte apoptosis, thus establishing a link between pressure overload and left ventricular (LV) remodelling., Methods and Results: Peak diastolic coronary blood flow velocity (CBFV) was evaluated at transthoracic Doppler echocardiography, and signal intensity (SI) and the rate of SI rise (beta) were measured at myocardial contrast echocardiography in 11 patients with severe aortic stenosis and LV hypertrophy. In the same patients, biopsies were obtained from the anterolateral LV free wall during surgery and analysed for cardiomyocyte apoptosis. LV mass corrected CBFV (CBFVI) was significantly lower in patients than in controls (median 0.100 cm.g/s (interquartile range 0.07-0.115) v 0.130 cm.g/s (0.130-0.160), p = 0.002). Similarly, SI*beta was significantly lower in patients than in controls (11 1/s (8-66) v 83 1/s (73-95), p = 0.001). Apoptotic rate was increased in aortic stenosis more than 100-fold versus controls (1.2% (0.8-1.4) v 0.01% (0.01-0.01), p < 0.001) and inversely correlated with lower CBFVI and SI*beta (r = -0.77, p = 0.001 for both)., Conclusions: Patients with severe aortic stenosis and LV hypertrophy have impaired myocardial perfusion, which is associated with enhanced cardiomyocyte apoptosis. Impaired myocardial perfusion and the ensuing oxygen demand-supply imbalance may, at least partially, be responsible for increased apoptosis and possible transition to heart failure, thus establishing a link between pressure overload, LV remodelling, and heart failure.

Objective: To identify in humans the temporal patterns of no reflow and their functional implications., Methods: 24 patients with first acute myocardial infarction and successful coronary recanalisation by recombinant tissue-type plasminogen activator (n = 15) or primary percutaneous transluminal coronary angioplasty (n = 9) were studied by myocardial contrast echocardiography within 24 hours of recanalisation and at one month's follow up. Myocardial contrast echocardiography was performed by intermittent harmonic power Doppler and intravenous Levovist. The regional contrast score index (CSI) was calculated within dysfunctioning myocardium. Videointensity was measured (dB) within risk and control areas and their ratio was calculated., Results: In 8 patients reflow was observed at 24 hours and persisted at one month. Conversely in 16 patients areas of no reflow were detectable at 24 hours. At one month, no reflow was spontaneously reversible in 9 patients (mean (SD) CSI and videointensity ratio improved from 2.5 (0.5) to 1.4 (0.6) and from 0.6 (0.1) to 0.7 (0.1), respectively; p < 0.05) and was sustained in the remaining 7 patients (CSI and videointensity ratio remained unchanged from 2.6 (0.6) to 2.6 (0.5) and from 0.5 (0.2) to 0.5 (0.2), respectively; NS). Left ventricular function improved significantly in patients with reflow and reversible no reflow. Volumes were enlarged only in patients with sustained no reflow., Conclusions: No reflow detected at 24 hours may be sustained or spontaneously reversible at one month. Such reversibility of the phenomenon is associated with preserved left ventricular volumes and function. Clarification of the mechanisms of delayed reversibility may lead to tailored treatment of no reflow even in the subacute phase of myocardial infarction.