Articles

Objective: To investigate in an animal model of Pulmonary Hypertension (PH) by monocrotaline whether a lower exercise intensity, which has lower potential to provoke dyspnea symptoms, could prevent the increase the right ventricle pressure and the decrease in respiratory compliance. Setting: A research laboratory. ANIMALS: twenty-one Wistar rats were randomized to the groups: Control (CO; saline solution); PH-sedentary; PH-low and PH-moderate intensity of exercise training (ET). Interventions: They received a single saline or monocrotaline subcutaneous injection (50 mg/kg). The exercise program was performed during 3-weeks. Main Outcome Measures: Rats were evaluated by their morphometric and hemodynamic changes and by the respiratory mechanic responses induced by the exercise protocols. Results: Both protocols of ET significantly (p < 0.05) attenuated the increase in the right ventricular systolic pressure. However, the lower intensity was more effective to prevent the impairment in the respiratory and quasi-static compliance. Conclusion: Collectively, our results showed for the first time the benefits of ET to the respiratory system mechanics. We also demonstrated that intensity is crucial in PH, probably due to the difficulty to match VO2 capacity and O2 demand during exercise. The improvement in quasi-static compliance not only might improve the ability to breathe, and capture oxygen, but also welfare.

A key platform underpinning the traditional understanding of the cardiovascular system, with respect to the behavior of large arterial vessels, is Otto Frank’s Windkessel Hypothesis [1]. This hypothesis posits simply that the smooth muscle walls of large arteries do not undergo rhythmic contractions in synchrony with the heartbeat but, rather, behave as passive elastic tubes undergoing distension from pulsatile pressure waves. The Windkessel Hypothesis is elegant, well described for over a century, ingrained in the understanding of cardiovascular medicine and physiology, and simply wrong. Several groups have now shown that the arterial smooth muscle wall undergoes rhythmic activation in synchrony with the heartbeat in a variety of tissues, including human brachial artery; canine coronary, femoral, and carotid arteries; rabbit aorta; feline pulmonary artery and rodent aorta [2-8]. The phasing of these events is such that the upstroke of the contraction slightly precedes the upstroke of the pulse wave, suggesting nomenclature for the events as pulse synchronized contractions, or PSCs [3,6-8]. PSCs have been found to be of neurogenic origin, sensitive to the neural blocker tetrodotoxin [3,8]. Although the specific neural pathways regulating PSCs have not been elucidated, the alpha-adrenergic system is at least partially involved, as evidenced by reduction or blockade of PSCs by the alpha-adrenergic blocker phentolamine [8]. Further, PSCs have not been observed following vessel excision in in vitro studies, as an intact nervous system is not present. The pacemaker for the PSC resides in the right atrium, as suggested by two lines of evidence. First, pacing of the right atrial region to faster than spontaneous frequencies leads to a one-to-one correspondence of PSC frequency with the stimulation rate [3]. Additionally, excision of the right, but not the left, atrial appendage results in elimination of PSCs [3]. As the pacemaker region for PSCs and the heartbeat both lie in the right atrium, this may potentially allow for coordination between the heartbeat and pulse wave with PSCs [3,5,8]. Extensive evaluations also have been performed showing the PSC was not an artifact produced either by cardiac contractility or from the vessel distension from the pulse wave [3,5,6].

Background: Contrast-induced acute kidney injury (CI-AKI) is an important cause of increasing the hospital stay and in-hospital mortality. By increasing intra-renal vasoconstriction, left ventricular ejection fraction (LVEF) can increase the risk of CI-AKI. We sought to investigate whether LVEF can impact the incidence of CI-AKI after cardiac catheterization and whether it can be used to predict CI-AKI. Methods: Patients underwent cardiac catheterization from December 2017 to February 2018 at Jersey Shore University Medical Center were enrolled in the study. Contrast-induced acute kidney injury (CI-AKI) was defined as an increase in serum creatinine of ≥ 0.5 mg/dL or an increase of ≥ 25% from the pre-procedure value within 72 hours post-procedure. The maximum allowable contrast dose was calculated using the following formula: (5* (weight (kg)/creatinine level (mg/dL)). A multivariable logistic regression analyses, controlling for potential confounders, were used to test associations between LVEF and CI-AKI. Results: 9.6% had post catheterization CI-AKI. A total of 18 out of 44 (44%) of patients who had CI-AKI also had ongoing congestive heart failure. No statistically significant association found neither with maximum allowable contrast (p = 0.009) nor ejection fraction (p = 0.099) with the development of CI-AKI. Conclusion: In spite of the fact that no statistically significant relationship found between the percentage maximum contrast dose and the ejection fraction with the post-procedure CI-AKI, we heighten the essential of employing Maximum Allowable Contrast Dose (MACD) and ejection fraction in patients undergoing PCI to be used as a clinical guide to predict CI-AKI.

Background: Subclavian venous access for pacemaker lead insertion is a common procedure and is normally considered safe in the hands of an expert. However, subclavian venepuncture is not without complications, starting from mild subcutaneous hematoma to pneumothorax. We here present a case of hemoptysis occurring after difficult subclavian vein puncture, which subsequently improved on conservative management only. Case Summary: A 65-year-old gentleman, post aortic valve replacement had persistent high-grade AV block and was taken up for a dual chamber pacemaker implantation. Immediately following venous access, he had a bout of hemoptysis, which recovered on its own. Post procedure chest x-ray was suggestive of alveolar hemorrhage which cleared gradually in next three-four days. Discussion: Post subclavian venepuncture hemoptysis is known; but it is a rare complication, arising either because of lung parenchyma injury or arterial injury. This is mostly benign and improves on conservative management only; however rarely it may be massive and life threatening where transcatheter arterial embolization may be required.

Background: Hypertrophic cardiomyopathy (HCM) patients have a predisposition for malignant VT/VF and consequently, sudden cardiac death (SCD). In single center studies, late gadolinium enhancement (LGE) defined fibrosis has been linked to VT/VF. However, despite innumerable investigations, SCD has not been definitely attributable to LGE. Explanations for these are believed to be related to insufficient statistical power. Methods: We performed an electronic search of MEDLINE, PubMed: and CMR abstracts for original data published or presented between Jan 2001 to Mar 2011. Key search terms: HCM, LV fibrosis, SCD and LGE. Studies were screened for eligibility based on inclusion criteria: referral for CMR exam with LGE for HCM; and follow-up for incidence of VT/VF and SCD. Categorical variables were evaluated between patient groups via Chi-square test. Results: A total of 64 studies were initially identified. Of these, 4 (6.3%) were identified and included (n = 1063 patients). Three prospective and one retrospective study were included. LGE was detected in 59.6% of patients. As expected, the presence of myocardial fibrosis was associated with VT/VF (x2 = 6.5, p < 0.05; OR 9.0, (95% CI 1.2 to 68.7). Moreover, myocardial fibrosis strongly predicted SCD (x2 = 6.6, p < 0.05; OR 3.3 (95% CI 1.2 to 9.7). Conclusion: Despite single center CMR studies, LGE has consistently predicted VT/VF while prediction of SCD has remained paradoxically unlinked. Although the lack of studies meeting our criteria limited our ability to perform a comprehensive meta-analysis, we have been able to demonstrate for the first time that LGE-defined fibrosis is a predictor of SCD in patients with HCM0.

Chronic heart failure has been extensively characterized as a disorder arising from a complex interaction between impaired ventricular performance and neurohormonal activation. Since beta adrenoceptor blocking agents are currently considered an integral component of therapy for the management of patients with severe chronic heart failure; several well designed clinical trials have been conducted to determine the morbidity and mortality benefits of these agents these studies, however did not yield the same results in terms of morbidity and mortality benefits. Currently only Bisoprolol, Carvedilol and sustained release metoprolol succinate have clinically proven and convincing morbidity and mortality benefits the current list of approved medicines of the National Health Insurance Scheme (NHIS) of the republic of Ghana does not provide coverage for these lifesaving therapeutic agents. The objective of this review was to collate the relevant scientific evidence that will convince the authorities at the National Health Insurance Authority (NHIA) of the Republic of Ghana to include at least one of the evidence based beta adrenoceptor blocking agents in the list of approved medicines. A thorough search on the internet was conducted using Google scholar to obtain only the clinically relevant studies associated with the benefits of beta adrenoceptor blocking agents in patients with chronic heart failure published in the English language. The phrases beta adrenoceptor blocking agents and chronic heart failure were used as search engines. The search engine yielded several studies that met the predefined inclusion criteria. However, only the Cardiac Insufficiency BIsoprolol Studies (CIBIS-I and CIBIS-II), Carvedilol Prospective Randomized Cumulative Survival Study (COPERNICUS) and Metoprolol CR/XL Randomized Intervention Trial (MERIF-HF) because of the clinical relevance of their findings Beta adrenoceptor blocking agents such as atenolol and propranolol have been used in the management of patients with chronic heart failure. However, their efficacy and optimal dose in reducing mortality have not been scientifically established not all beta adrenoceptor blocking agents scientifically studied provide the same degree of clinically meaningful and convincing morbidity and mortality benefits in patients with chronic heart failure.

Critical congenital heart defects (CCHDs) are preferably diagnosed prenatally or soon after birth. Late diagnosis has been related to poorer prognosis. The aim of this study is to assess when CCHDs are diagnosed in Iceland and whether late diagnosis is a problem. All live born children in Iceland and foetuses diagnosed with CCHDs during the years 2000-2014 were included. CCHD was defined as a defect requiring intervention or causing death in the first year of life, or leading to abortion. The total number of pre- and postnatal diagnosis of CCHDs was 188. Prenatal diagnosis was made in 69 of 188 (36.7%). Of 69 diagnosed prenatally 33 were terminated due to CCHD. Of the 155 live born children with CCHD, 36 (23.2%) had a prenatal diagnosis and 100 (64.5%) were diagnosed shortly after birth, before discharge from birth facility. 19 children (12.3%) were diagnosed late, that is after discharge from birth facility. Coarctation of the aorta was the most common CCHD diagnosed late (6/19). Prenatal screening and newborn examination give good results in diagnosis of CCHDs in Iceland. Late diagnosis are relatively few, but both the number of prenatally diagnosed CCHDs and CCHDs diagnosed shortly after birth can be further improved.

Objective: The aim of this study was to estimate the predictive clinical value of CHA2DS2-VASc score for no-reflow phenomena in patients having ST-segment elevation myocardial infarction (STEMI) who applied to primary percutaneous coronary intervention (PCI). Subjects and Methods: Three-hundred STEMI patients underwent primary PCI. They were classified into: group (1) included 27 patients with no-reflow and group (2) included 273 patients without no-reflow (control). CHA2DS2-VASc risk score was computed for each patient. Results: This study found statistically significant difference (p < 0.05) in multivariate analysis of the association between CHA2DS2-VASc score and no-reflow phenomenon. The predictive power of individual components in CHA2DS2-VASc score for no-reflow was statistically significant difference (p < 0.05). So, significantly higher CHA2DS2-VASc score is connected with higher risk of no-reflow and in-hospital mortality rate. Conclusion: Significantly higher CHA2DS2-VASc score is associated with higher risk of no- reflow phenomenon and in-hospital mortality rates in patients with STEMI who underwent primary PCI.

Purpose: This study reports resource utilization during a Medicare Beneficiary’s (MBs) Transcatheter Aortic Valve Replacement (TAVR) index hospitalization and all subsequent encounters for 12 months and compares data between MBs who did or did not receive a pacemaker implantation (PPM) during their index hospitalization. Method: This retrospective study examined Medicare hospital claims from January 1, 2014 through June 30, 2015. 15,533 MBs who survived for 365 days were studied. Information from all encounters during the study period was combined to compare hospital resource utilization and outcomes. Results: 14.8% of MBs had a PPM during the index hospitalization. 46.0% of MBs had at least one readmission to a hospital during the 365-day follow-up period. 54.6% of MB’s first hospital readmission occurred within 90 days of their TAVR discharge date. Average total Medicare reimbursement for all hospitalizations was $60,638 ± $28,974 associated with average total hospital length of stay of 11.2 ± 11.7 days. After adjusting for demographics and 47 comorbid conditions, MBs receiving a PPM during the index TAVR had significantly higher estimated Medicare reimbursement ($5,132) and longer total length of stay (1.8 days) for the entire study period than MBs not receiving a PPM. Conclusion: Total Medicare reimbursement and hospital LOS were significantly higher among MBs that had a PPM implantation during their index admission; however, there were no significant differences in readmission rates, readmission length of stay, or days to first readmission during the follow-up period between the two study cohorts.

Background: Anemia is an accelerating problem among patients with heart failure (HF) and its presence is associated with more symptoms. In this study, we investigated whether anemia in heart failure was related to hepcidin concentration. Methods: 50 patients with heart failure and 20 healthy subjects with no history of a chronic illness including heart failure as control group, were included in the study. Heart failure was verified by echocardiography in each subject and patients were defined as ones with reduced ejection fraction (HFrEF) if EF ≤ 40% and with preserved ejection fraction (HFpEF) if EF 40% - 50%. Blood samples were taken from all patients after 10-12 hours fasting. Anemia assessment was performed according to World Health Organization (WHO) criterias. Results: There was a positive correlation between hepcidin concentration and urea, ferritin, hemoglobin, hematocrite, C-reactive protein (p < 0,05). Hepcidin concentrations of anemic heart failure patients were significantly lower than the non-anemic heart failure patients (p < 0,05). Conclusion: We found that serum hepcidin concentration in anemic patients with heart failure was lower than in heart failure patients without anemia. We believe that iron defiency occurs as a result of inflammatory process in heart failure and therefore hepcidin concentrations decrease as a response. However, long-term follow up studies are needed.