Myocardial work in patients with heart failure and ischemic cardiomyopathy according to the mode of coronary revascularization.

BACKGROUND: The association of percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) on myocardial function, as reflected in myocardial work (MyW) parameters, in patients with ischemic cardiomyopathy and heart failure (HF) is unknown. METHODS: We analyzed data from 68 patients who were hospitalized with chronic HF due to ischemic cardiomyopathy and stratified them according to the mode of revascularization. All patients underwent a 2D speckle tracking echocardiography exam performed by the same expert sonographer and had complete MyW data including global work index (GWI), global constructive work (GCW), global wasted work (GWW), and global work efficiency (GWE). RESULTS: The mean age of patients was 70 ± 10 years and 86.8% were men. The mean left ventricular ejection fraction (LVEF) in overall cohort was 31.6 ± 9.5%. Both subgroups did not significantly differ in terms of baseline LVEF, comorbidities, and pharmacotherapy. Compared with those who received PCI, patients revascularized with CABG had significantly greater GWI (821 vs. 555 mmHg%, p = 0.002), GCW (1101 vs. 794 mmHg%, p = 0.001), GWE (78 vs. 72.6%, p = 0.025), and global longitudinal strain (-8.7 vs. -6.7%, p = 0.004). Both patient subgroups did not significantly differ with respect to GWW (273 vs. 245 mmHg%, p = 0.410 for CABG and PCI, respectively) and survival during the median follow-up of 18 months (log-rank p = 0.813). CONCLUSION: Patients with HF and ischemic cardiomyopathy revascularized with CABG had greater myocardial work performance when compared with those revascularized with PCI. This might suggest a higher degree of functional myocardial revascularization associated with the CABG procedure.

Emerging Therapies for the Treatment of Atherosclerotic Cardiovascular Disease: From Bench to Bedside.

Primarily a consequence of sedentary lifestyle, atherosclerosis has already reached pandemic proportions, and with every year the burden of it is only increasing. As low-density lipoprotein cholesterol (LDL-C) represents a crucial factor in atherosclerosis formation and progression, stringent lipid-lowering therapy could conceivably be the key to preventing the unfavorable outcomes that arise as a consequence of atherosclerosis. The use of statins in lipid-lowering is often burdened by adverse events or is insufficient to prevent cardiovascular events as a monotherapy. Therefore, in the present review, the authors aimed to discuss the underlying mechanisms of dyslipidemia and associated atherosclerotic cardiovascular disease (ASCVD) and preclinical and clinical trials of novel therapeutic approaches to its treatment, some of which are still in the early stages of development. Apart from novel therapies, a novel change in perspective is needed. Specifically, the critical objective in the future management of ASCVD is to embrace emerging evidence in the field of atherosclerosis, because clinicians are often burden by common practice and personal experience, both of which have so far been shown to be futile in the setting of atherosclerosis.

Conservative Management of Spontaneous Left Main Coronary Artery Dissection (SCAD) Triggered by Emotional Stress in the Late Postpartum Period: Case Report and Pathophysiology.

A spontaneous coronary artery dissection (SCAD) during the postpartum period is a serious medical emergency and the most important non-atherosclerotic cause of coronary artery disease (CAD) in this population. While conservative management is recommended in most SCAD scenarios, cases complicated by hemodynamic instability or cardiogenic shock are particularly challenging and might be amenable only with invasive percutaneous or cardiothoracic surgical management. Herein, we present a case of a 35-year-old otherwise healthy woman that suffered an intense emotional stress event and was subsequently admitted with crushing chest pain to the emergency department. The initial electrocardiogram showed dynamic changes suggesting anterolateral ST-elevation myocardial infarction. She gave birth to a healthy child 3 months before the current presentation. Diagnostic angiography found no occlusive CAD but instead an extensive intramural hematoma originating from the left main artery dissection and extending to the whole left coronary circulation was observed. Hemodynamic instability and hypotension soon followed, and the patient went into cardiogenic shock. The heart team opted for conservative and supportive intensive care management without surgical or percutaneous intervention. This decision ultimately led to the successful extubation of the patient and the achievement of hemodynamic stability. The patient was eventually safely discharged home without any permanent disability.

LEFT LATERAL VIEW FOR PCI TREATMENT OF INFERIOR STEMI IN A PATIENT WITH DEXTROCARDIA.

Rapid recognition of ST-segment elevation myocardial infarction and electrocardiogram interpretation in patients with dextrocardia could be a challenging situation. This case report discusses presentation in a patient with dextrocardia and situs inversus who was found to have acute inferior myocardial infarction. Percutaneous coronary intervention in cases of dextrocardia can be technically challenging considering coronary origin and orientation, and difficulty in appropriate catheter selection.

CONCURRENT DEEP VEIN THROMBOSIS AND PULMONARY EMBOLISM ASSOCIATED WITH HYPERTHYROIDISM: A CASE REPORT.

Numerous disorders of coagulation and fibrinolysis have been reported in patients with thyroid diseases, especially with hyperthyroidism. Most articles are focused on deep vein thrombosis risk, however, few of them describe association between hyperthyroidism and pulmonary embolism. We report a case of a 43-year-old woman with long-term uncontrolled hyperthyroidism complicated by venous thromboembolism. The potential mechanisms could be endothelial dysfunction, decreased fibrinolytic activity, and increased levels of coagulation factors. Thyroid evaluation should be recommended in patients with unprovoked venous thromboembolic events.

Feasibility and safety of catheter-directed thrombolysis via superficial cubital vein for the treatment of acute massive and submassive pulmonary embolism.

INTRODUCTION: Proximal venous approaches (femoral or jugular) for catheter-directed thrombolysis (CDT) of acute pulmonary embolism (PE) dominate in clinical practice. AIM: We investigated the feasibility and safety of CDT in acute PE by using the superficial cubital venous approach. MATERIAL AND METHODS: All patients with acute PE received intravenous unfractionated heparin plus CDT. CDT included mechanical thrombus fragmentation and the local application of adjuvant thrombolytic therapy through the pigtail catheter - alteplase administered as 2.5 mg bolus in each main branch of the pulmonary artery plus adjuvant 25 mg for 12 h in the more severely affected branch of the pulmonary artery. RESULTS: Twenty-seven consecutive patients presenting with acute massive (high risk) PE (n = 10) or submassive (intermediate risk) PE (n = 17) were enrolled in the study. The mean age of the enrolled cohort was 60.6 (14.1) years and most patients were female (n = 14, 52%). The procedural success of CDT application through the cubital vein was achieved in all patients. After the procedure, the systolic pulmonary artery pressure decreased from 61.4 (18.3) to 35.8 (12.3) mm Hg (p < 0.001) while the mean pulmonary artery pressure decreased from 35.7 (10.8) to 21.1 (6.5) mm Hg (p < 0.001). Similarly, the mean arterial pressure increased from 81.9 (12.8) to 89.0 (10.3) mm Hg (p = 0.031). Miller angiographic obstruction score and Miller index decreased significantly after the CDT intervention (p < 0.001). There were no deaths, major bleeding events, or hemorrhagic strokes. CONCLUSIONS: CDT by using the cubital approach is a simple, safe, and feasible treatment option for PE. This approach was associated with significant improvement in hemodynamic parameters without fatal outcomes or major periprocedural complications.

Bronchoalveolar pH and inflammatory biomarkers in patients with acute exacerbation of chronic obstructive pulmonary disease.

OBJECTIVES: This study aimed to directly measure pH in the lungs, determine lactate dehydrogenase (LDH), C-reactive protein (CRP), and glucose levels in serum and bronchoalveolar aspirate, and identify bacterial pathogens from bronchoalveolar fluid during acute exacerbation of chronic obstructive pulmonary disease (AECOPD). METHODS: We performed an observational, analytical case-control study from February 2015 to March 2017. We included 84 patients with AECOPD and 42 with stable chronic obstructive pulmonary disease (COPD). All participants underwent detailed medical anamnesis, a clinical examination, chest radiography, spirometry, an arterial blood gas test, bronchoscopy, bacterial culture, and serum/bronchiolar aspirate laboratory testing. RESULTS: The mean pH of bronchoalveolar fluid was significantly higher in patients with AECOPD than in patients with stable COPD. The mean lung pH value, bronchoalveolar and serum LDH levels, and serum CRP levels in patients with isolated bacteria were higher than those in patients without isolated bacteria in the AECOPD patient group. Lung pH values in patients with AECOPD were significantly correlated with bronchoalveolar LDH and glucose levels. CONCLUSIONS: AECOPD is associated with local cell and tissue injury in the lungs, especially in the presence of bacterial pathogens, which is accompanied by a low systemic inflammatory response.

Early Changes in Platelet Size and Number in Patients with Acute Coronary Syndrome.

A strong relationship exists between acute coronary syndrome (ACS) and platelets (PLTs) volume. Mean platelet volume (MPV) is a parameter of PLT functions and a marker for increased PLT activation. The aim of this study was to determine early changes in number of total PLT and MPV in different manifestation of ACS and to find out predictive value of MPV in the spectrum of ACS. This was a prospective study. One hundred thirty-four ACS patients were enrolled, 76 of them finished the study. PLT and MPV in patients with unstable angina, non-ST elevation, and ST elevation myocardial infarctions were determined on arrival and 1, 3, 72 hours, and 7 days after the admission to hospital. There was decrease in PLT and MPV in all three groups after 3 hours of arrival in hospital in comparison with admission values. In the later time period (72 hours and 7 days), there was an increase in PLT and MPV only in patients with acute myocardial infarction (AMI). We have revealed completely new dynamics in early changes in MPV and PLT count in patients with AMI. Biphasic changes were found in early phase after admission to the hospital. Fast response in these parameters raises new questions about their origin.

Cardiac Tamponade after Right Ventricular Perforation Caused by Screw-in Lead.

A 69-year-old man was admitted after syncope followed with chest pain and signs of cardiac tamponade. He had undergone permanent dual-chamber pacemaker implantation 3 weeks earlier. Transthoracic echocardiography (TTE) confirmed a pericardial effusion, and urgent pericardial drainage was performed. Right ventricular perforation caused by active-fixation (screw-in) lead was verified by multislice computed tomography. The lead was extracted under fluoroscopy and bedside TTE monitoring in the operating room with cardiothoracic surgery backup. In the same act, the new ventricular passive-fixation lead was implanted.

Resting arterial hypoxaemia in subjects with chronic heart failure, pulmonary hypertension and patent foramen ovale.

NEW FINDINGS: What is the central question of this study? Does a patent foramen ovale contribute to resting arterial hypoxaemia, defined as arterial oxygen saturation <95%, in subjects with chronic heart failure with or without pulmonary arterial hypertension? What is the main finding and its importance? The presence of a patent foramen ovale contributed to resting arterial hypoxaemia only in subjects with chronic heart failure with pulmonary arterial hypertension. These data suggest that the presence of a patent foramen ovale should be considered in chronic heart failure patients with arterial hypoxaemia and pulmonary hypertension. The roles of intrapulmonary and intracardiac shunt in contributing to arterial hypoxaemia at rest in subjects with chronic heart failure (CHF) have not been well investigated. We hypothesized that blood flow through intrapulmonary arteriovenous anastomoses (Q̇ IPAVA ) and/or patent foramen ovale (Q̇ PFO ) could potentially contribute to arterial hypoxaemia and, with pulmonary hypertension (PH) secondary to CHF, this contribution may be exacerbated. Fifty-six subjects with CHF (New York Heart Association Classes I-III), with (+) or without (-) PH [defined as peak tricuspid regurgitation velocity ≥2.9 m s(-1) (CHF PH+, n = 32) and peak tricuspid regurgitation velocity ≤2.8 m s(-1) (CHF PH-, n = 24)], underwent arterial blood gas analysis and transthoracic saline contrast echocardiography concomitant with transcranial Doppler to detect Q̇ IPAVA and Q̇ PFO . Seventeen of 56 subjects with CHF (30%) had Q̇ PFO , but only four of 56 subjects with CHF had Q̇ IPAVA (7%), both similar to age- and sex-matched control subjects. Mean arterial oxygen saturation (SaO2) was lower in subjects with Q̇ PFO . Only CHF PH+ subjects with Q̇ PFO had arterial hypoxaemia (mean SaO2 <95%). Bubble scores assessed using transthoracic saline contrast echocardiography were correlated with microembolic signals detected with transcranial Doppler in subjects with Q̇ PFO . Significant Q̇ IPAVA was not present in either CHF PH+ or PH- subjects, suggesting that Q̇ IPAVA is not dependent on increased pulmonary pressure and does not contribute significantly to arterial hypoxaemia in older subjects with CHF. Given that SaO2 was lower in all subjects with CHF who had Q̇ PFO compared with those without Q̇ PFO , a patent foramen ovale should be considered when determining potential causes of arterial hypoxaemia, because Q̇ PFO was present in 30% of these subjects.

Tracheomalatia, to stent or not to stent.

Benign thyroid disorders such as goiter, especially retrosternal, can cause tracheostenosis by extrinsic tracheal compression, which is due to the lack of specific symptoms often misdiagnosed. Tracheomalatia develops as a result to long term tracheal compression and refers to weakness of the trachea characterized by softness of the tracheal cartilage arches and by loss of regular tracheal structure. Tracheomalatia is characterized by reduction of the endotracheal lumen and may affect the entire trachea or may be localized to one portion of it. We present the case of a 72-year old patient with distinct tracheostenosis and tracheomalatia, caused by long term pressure by the retrosternal goiter. We have been monitoring the patient for last 20 years after the second endotracheal stent had been placed. The first one was placed 34 years ago, in 1981. On both occasions granulation tissue and colonization of bacteria occurred. In the end the placed stents were rejected and migrated to the main carina. Despite the tracheal diameter narrower than 5 mm the patient has been living normally without the stent for 17 years, with the exception of no hard physical labor. He had a few short term antibiotic therapies and bronchial toilets during symptomatic deteriorations. Diagnosing retrosternal goiter and surgical treatment on time is of crucial importance in cases such as this one. Considering the complications caused by the stent, our opinion is that the majority of patients may require conservative treatment with closely monitoring during respiratory infections.

The impact of consecutive freshwater trimix dives at altitude on human cardiovascular function.

Self-contained underwater breathing apparatus (SCUBA) diving is regularly associated with numerous asymptomatic changes in cardiovascular function. Freshwater SCUBA diving presents unique challenges compared with open sea diving related to differences in water density and the potential for dive locations at altitude. The aim of this study was to evaluate the impact of freshwater trimix diving at altitude on human cardiovascular function. Ten divers performed two dives in consecutive days at 294 m altitude with the surface interval of 24 h. Both dives were at a depth of 45 m with total dive time 29 and 26 min for the first and second dive, respectively. Assessment of venous gas embolization, hydration status, cardiac function and arterial stiffness was performed. Production of venous gas emboli was low, and there were no significant differences between the dives. After the first dive, diastolic blood pressure was significantly reduced, which persisted up to 24 h. Left ventricular stroke volume decreased, and heart rate increased after both dives. Pulse wave velocity was unchanged following the dives. However, the central and peripheral augmentation index became more negative after both dives, indicating reduced wave reflection. Ejection duration and round trip travel time were prolonged 24 h after the first dive, suggesting longer-lasting suppression of cardiac and endothelial function. This study shows that freshwater trimix dives with conservative profiles and low venous gas bubble loads can result in multiple asymptomatic acute cardiovascular changes some of which were present up to 24 h after dive.

Phantom tumor of the lung: localized interlobar effusion in congestive heart failure.

Localized interlobar effusions in congestive heart failure (phantom or vanishing lung tumor/s) is/are uncommon but well known entities. An 83-year-old man presented with shortness of breath, swollen legs, and dry cough enduring five days. Chest-X-ray (CXR) revealed massive sharply demarked round/oval homogeneous dense shadow 10 × 7 cm in size in the right inferior lobe. The treatment with the loop diuretics and fluid intake reduction resulted in complete resolution of the observed round/oval tumor-like image on the control CXR three days later. Radiologic appearance of such a mass-like configuration in patients with congestive heart failure demands correction of the underlying heart condition before further diagnostic investigation is performed to avoid unnecessary, expensive, and possibly harmful diagnostic and treatment errors.

The effects of nitroglycerin, norepinephrine and aminophylline on intrapulmonary arteriovenous anastomoses in healthy humans at rest.

We have investigated the effects of the intravenous infusion of nitroglycerin (NTG), norepinephrine (NE) and aminophylline (AMP) on the opening and recruitment of intrapulmonary arteriovenous anastomoses (IPAVA) in healthy humans at rest. In ten volunteers saline contrast echocardiography was performed during administration of two doses of the NTG (3µgkg(-1)min(-1) and 6µgkg(-1)min(-1)) and NE (0.1µgkg(-1)min(-1) and 0.25µgkg(-1)min(-1)) as well as 30min following the administration of AMP at rate of 6mgkg(-1). Echocardiography was used to assign bubble scores (0-5) based on the number and spatial distribution of bubbles in the left ventricle. Doppler ultrasound was used to estimate pulmonary artery systolic pressure. Using a Finometer the following hemodynamic parameters were assessed: heart rate, stroke volume, cardiac output, total peripheral resistance as well as systolic, diastolic and mean arterial pressure. The most important finding from the current study was that nitroglycerin, norepinephrine and aminophylline in the applied doses were not found to promote IPAVA opening in healthy humans at rest.