Left ventricular reverse remodelling and its predictors in non-ischaemic cardiomyopathy.

Adverse remodelling following an initial insult is the hallmark of heart failure (HF) development and progression. It is manifested as changes in size, shape, and function of the myocardium. While cardiac remodelling may be compensatory in the short term, further neurohumoral activation and haemodynamic overload drive this deleterious process that is associated with impaired prognosis. However, in some patients, the changes may be reversed. Left ventricular reverse remodelling (LVRR) is characterized as a decrease in chamber volume and normalization of shape associated with improvement in both systolic and diastolic function. LVRR might occur spontaneously or more often in response to therapeutic interventions that either remove the initial stressor or alleviate some of the mechanisms that contribute to further deterioration of the failing heart. Although the process of LVRR in patients with new-onset HF may take up to 2 years after initiating treatment, there is a significant portion of patients who do not improve despite optimal therapy, which has serious clinical implications when considering treatment escalation towards more aggressive options. On the contrary, in patients that achieve delayed improvement in cardiac function and architecture, waiting might avoid untimely implantable cardioverter-defibrillator implantation. Therefore, prognostication of successful LVRR based on clinical, imaging, and biomarker predictors is of utmost importance. LVRR has a positive impact on prognosis. However, reverse remodelled hearts continue to have abnormal features. In fact, most of the molecular, cellular, interstitial, and genome expression abnormalities remain and a susceptibility to dysfunction redevelopment under biomechanical stress persists in most patients. Hence, a distinction should be made between reverse remodelling and true myocardial recovery. In this comprehensive review, current evidence on LVRR, its predictors, and implications on prognostication, with a specific focus on HF patients with non-ischaemic cardiomyopathy, as well as on novel drugs, is presented.

Screening and Risk Stratification Strategy Reduced Decompression Sickness Occurrence in Divers With Patent Foramen Ovale.

OBJECTIVES: This paper sought to evaluate the occurrence of decompression sickness (DCS) after the application of a patent foramen ovale (PFO) screening and risk stratification strategy. BACKGROUND: PFO is associated with an increased risk of DCS. Recently, transcatheter closure was reported to reduce DCS occurrence in divers with a high-grade shunt. However, to date, there are no data regarding the effectiveness of any PFO screening and risk stratification strategy for divers. METHODS: A total of 829 consecutive divers (age 35.4 ± 10.0 years, 81.5% men) were screened for PFO by means of transcranial color-coded sonography in the DIVE-PFO (Decompression Illness Prevention in Divers with a Patent Foramen Ovale) registry. Divers with a high-grade PFO were offered either catheter-based PFO closure (the closure group) or advised conservative diving (high grades). Divers with a low-grade shunt were advised conservative diving (low grades), whereas those with no PFO continued unrestricted diving (controls). A telephone follow-up was performed. To study the effect of the screening and risk stratification strategy, DCS occurrence before enrollment and during the follow-up was compared. RESULTS: Follow-up was available for 748 (90%) divers. Seven hundred and 2 divers continued diving and were included in the analysis (mean follow-up 6.5 ± 3.5 years). The DCS incidence decreased significantly in all groups, except the controls. During follow-up, there were no DCS events in the closure group; DCS incidence was similar to the controls in the low-grade group (HR: 3.965; 95% CI: 0.558-28.18; P = 0.169) but remained higher in the high-grade group (HR: 26.170; 95% CI: 5.797-118.160; P < 0.0001). CONCLUSIONS: The screening and risk stratification strategy using transcranial color-coded sonography was associated with a decrease in DCS occurrence in divers with PFO. Catheter-based PFO closure was associated with a DCS occurrence similar to the controls; the conservative strategy had a similar effect in the low-grade group, but in the high-grade group the DCS incidence remained higher than in all other groups.

Carotid artery plaque composition and distribution: near-infrared spectroscopy and intravascular ultrasound analysis.

Most atherosclerotic plaques (APs) form in typical predilection areas of low endothelial shear stress (ESS). On the contrary, previous data hinted that plaques rupture in their proximal parts where accelerated blood flow causes high ESS. It was postulated that high ESS plays an important role in the latter stages of AP formation and in its destabilization. Here, we used near-infrared spectroscopy (NIRS) to analyse the distribution of lipid core based on the presumed exposure to ESS. A total of 117 carotid arteries were evaluated using NIRS and intravascular ultrasound (IVUS) prior to carotid artery stenting. The point of minimal luminal area (MLA) was determined using IVUS. A stepwise analysis of the presence of lipid core was then performed using NIRS. The lipid core presence was quantified as the lipid core burden index (LCBI) within 2 mm wide segments both proximally and distally to the MLA. The analysed vessel was then divided into three 20 mm long thirds (proximal, middle, and distal) for further analysis. The maximal value of LCBI (231.9 ± 245.7) was noted in the segment localized just 2 mm proximally to MLA. The mean LCBI in the middle third was significantly higher than both the proximal (121.4 ± 185.6 vs. 47.0 ± 96.5, P < 0.01) and distal regions (121.4 ± 185.6 vs. 32.4 ± 89.6, P < 0.01). Lipid core was more common in the proximal region when compared with the distal region (mean LCBI 47.0 ± 96.5 vs. 32.4 ± 89.6, P < 0.01).

Nonpharmacological Treatment of Atrial Fibrillation: What Is the Role of Device Therapy?

Atrial fibrillation is the most common arrhythmia in the adult population, and its incidence and prevalence are still rising. Cardiac devices are widely used in clinical practice in the management of various rhythm disturbances and heart failure treatment. Many patients who receive a pacemaker, implantable cardioverter-defibrillator, or cardiac resynchronization therapy also experience atrial fibrillation in the course of their life. Therefore, this review aims to describe the role of these devices in the treatment and prevention of atrial fibrillation in the device recipients. In addition, all these implantable devices also serve as permanent ECG (electrocardiogram) monitors, thus providing important information about the presence and characteristics of atrial fibrillation that may or may not be detected by the patient but can modify our therapeutical approach with regard to the stroke prevention.

MicroRNA-331 and microRNA-151-3p as biomarkers in patients with ST-segment elevation myocardial infarction.

We sought to analyse plasma levels of peripheral blood microRNAs (miRs) as biomarkers of ST-segment-elevation myocardial infarction (STEMI) due to type-1 myocardial infarction as a model situation of vulnerable plaque (VP) rupture. Samples of 20 patients with STEMI were compared both with a group of patients without angina pectoris in whom coronary angiogram did not reveal coronary atherosclerotic disease (no coronary atherosclerosis-NCA) and a group of patients with stable angina pectoris and at least one significant coronary artery stenosis (stable coronary artery disease-SCAD). This study design allowed us to identify miRs deregulated in the setting of acute coronary artery occlusion due to VP rupture. Based on an initial large scale miR assay screening, we selected a total of 12 miRs (three study miRs and nine controls) that were tested in the study. Two of the study miRs (miR-331 and miR-151-3p) significantly distinguished STEMI patients from the control groups, while ROC analysis confirmed their suitability as biomarkers. Importantly, this was observed in patients presenting early with STEMI, even before the markers of myocardial necrosis (cardiac troponin I, miR-208 and miR-499) were elevated, which suggests that the origin of miR-331 and miR-151-3p might be in the VP. In conclusion, the study provides two novel biomarkers observed in STEMI, which may be associated with plaque rupture.

High-grade patent foramen ovale is a risk factor of unprovoked decompression sickness in recreational divers.

BACKGROUND: Patent foramen ovale (PFO), male sex, age, and body mass index (BMI) were all identified as potential risk factors of decompression sickness (DCS). It has been debated whether PFO might cause unprovoked DCS (i.e. without violation of decompression procedure) due to paradoxical embolization of venous gas emboli. To date, there are no data on the incidence or risk factors of unprovoked DCS. This study sought to evaluate the risk factors of unprovoked DCS in recreational divers. METHODS: A total of 489 consecutive divers were screened for PFO between January 2006 and January 2014 by means of transcranial Doppler. All patients were prospectively included in the study registry. Survival analysis techniques were used to assess for risk factors for unprovoked DCS. Age, sex, BMI, PFO presence, and grade were analyzed. The total sum of dives was used as a measure of time. RESULTS: The group performed a total of 169,411 dives (mean 346±636). Thirty-six (7%) of the divers suffered from an unprovoked DCS. The frequency of PFO was 97.2% in divers with a history of unprovoked DCS and 35.5% in controls (p<0.001). There was no difference in sex, age, BMI, or total number of dives between the respective groups. In the adjusted Cox proportional hazards model, PFO grade 3 was a major risk factor for unprovoked DCS; there was a slight protective effect of increasing age. CONCLUSIONS: We demonstrated that a high-grade PFO was a major risk factor for unprovoked DCS in recreational scuba divers.

The role of near-infrared spectroscopy in the detection of vulnerable atherosclerotic plaques.

Coronary artery disease is the leading cause of mortality worldwide. Most acute coronary syndromes are caused by a rupture of a vulnerable atherosclerotic plaque which can be characterized by a lipid-rich necrotic core with an overlying thin fibrous cap. Many vulnerable plaques can cause angiographically mild stenoses due to positive remodelling, which is why the extent of coronary artery disease may be seriously underestimated. In recent years, we have witnessed a paradigm shift in interventional cardiology. We no longer focus solely on the degree of stenosis; rather, we seek to determine the true extent of atherosclerotic disease. We seek to identify high-risk plaques for improvement in risk stratification of patients and prevention. Several imaging methods have been developed for this purpose. Intracoronary near-infrared spectroscopy is one of the most promising. Here, we discuss the possible applications of this diagnostic method and provide a comprehensive overview of the current knowledge.

History and current use of mild therapeutic hypothermia after cardiac arrest.

In spite of many years of development and implementation of pre-hospital advanced life support programmes, the survival rate of out-of-hospital cardiac arrest (OHCA) used to be very poor. Neurologic injury from cerebral hypoxia is the most common cause of death in patients with OHCA. In the past two decades, post-resuscitation care has developed many new concepts aimed at improving the neurological outcome and survival rate of patients after cardiac arrest. Systematic post-cardiac arrest care after the return of spontaneous circulation, including induced mild therapeutic hypothermia (TH) in selected patients, is aimed at significantly improving rates of long-term neurologically intact survival. This review summarises the history and current knowledge in the field of mild TH after OHCA.

Intravascular Near-Infrared Spectroscopy: A Possible Tool for Optimizing the Management of Carotid Artery Disease.

Stroke is the second most common cause of morbidity and mortality in the Western nations. It is estimated that approximately one-fifth of all strokes or transient ischemic attacks are caused by carotid artery disease. Thus, treatment of carotid artery disease as a mean of stroke prevention is extremely important. Since the introduction of carotid endarterectomy, debate has persisted over the treatment strategy for carotid artery disease. Current recommendations have many potential flaws because they are often based on older trials performed before the introduction of modern pharmacotherapy and are mostly based on the angiographic degree of stenosis, without an emphasis on the pathophysiology of the disease. Most carotid events are caused by rupture or distal embolization of the content of an unstable atherosclerotic plaque with a large lipid pool. Thus, it is plausible that the information regarding the composition of the atherosclerotic plaque could play an important role in deciding on a treatment strategy. In this review article, we provide information about near-infrared spectroscopy, a new invasive imaging modality, which seems to be capable of providing such information.

Patent Foramen Ovale in Recreational and Professional Divers: An Important and Largely Unrecognized Problem.

Patent foramen ovale (PFO) is associated with an increased risk of decompression sickness (DCS) in divers that results from a paradoxical embolization of nitrogen bubbles. The number of scuba divers worldwide is estimated in the millions, and the prevalence of PFO is 25%-30% in adults. It is interesting that despite these numbers, many important issues regarding optimal screening, risk stratification, and management strategy still remain to be resolved. Recently published data suggest the possible effectiveness of both PFO closure and conservative diving measures in preventing arterial gas embolization. This review aims to introduce the basic principles of physiology and the pathophysiology of bubble formation and DCS, summarize the current literature on PFO and diving, and review the possibilities of diagnostic workup and management.

Effect of catheter-based patent foramen ovale closure on the occurrence of arterial bubbles in scuba divers.

OBJECTIVES: This study sought to evaluate the effect of catheter-based patent foramen ovale (PFO) closure on the occurrence of arterial bubbles after simulated dives. BACKGROUND: PFO is a risk factor of decompression sickness in divers due to paradoxical embolization of bubbles. To date, the effectiveness of catheter-based PFO closure in the reduction of arterial bubbles has not been demonstrated. METHODS: A total of 47 divers (age 35.4 ± 8.6 years, 81% men) with a PFO (PFO group) or treated with a catheter-based PFO closure (closure group) were enrolled in this case-controlled observational trial. All divers were examined after a simulated dive in a hyperbaric chamber: 34 divers (19 in the PFO group, 15 in the closure group) performed a dive to 18 m for 80 min, and 13 divers (8 in the PFO group, 5 in the closure group) performed a dive to 50 m for 20 min. Within 60 min after surfacing, the presence of venous and arterial bubbles was assessed by transthoracic echocardiography and transcranial color-coded sonography, respectively. RESULTS: After the 18-m dive, venous bubbles were detected in 74% of divers in the PFO group versus 80% in the closure group (p = 1.0), and arterial bubbles were detected in 32% versus 0%, respectively (p = 0.02). After the 50-m dive, venous bubbles were detected in 88% versus 100%, respectively (p = 1.0), and arterial bubbles were detected in 88% versus 0%, respectively (p < 0.01). CONCLUSIONS: No difference was observed in the occurrence of venous bubbles between the PFO and closure groups, but the catheter-based PFO closure led to complete elimination of arterial bubbles after simulated dives. (Nitrogen Bubble Detection After Simulated Dives in Divers With PFO and After PFO Closure; NCT01854281).

Left ventricular outflow tract obstruction after mitral valve repair treated with alcohol septal ablation.

Left ventricular outflow tract (LVOT) obstruction due to systolic anterior motion of the mitral valve (SAM) occurs in 4-5% of patients after mitral valve repair. If conservative treatment is unsuccessful, reoperation is indicated. Treatment options include repeated mitral valve repair or valve replacement and septal myectomy if hypertrophy is present. We report a case of a patient with pre-operatively undiagnosed hypertrophic cardiomyopathy who suffered from progressive dyspnea post-operation due to severe LVOT obstruction with SAM. This case was successfully treated with catheter-based alcohol septal ablation.