Cardiology (Cardiology)

Publications in this journal

• Article: Low-Dose Furosemide Administered with Adequate Hydration Reduces Contrast-Induced Nephropathy in Patients Undergoing Coronary Angiography.

  Guo-Qiang Gu, Rui Lu, Wei Cui, Fan Liu, Ying Zhang, Xiao-Hong Yang, Xue-Feng Chen, Wan-Ming Jia
  [show abstract] [hide abstract]
  ABSTRACT: Objective: We investigated the effects of low-dose furosemide, administered with adequate hydration on contrast-induced nephropathy (CIN). Methods: A total of 859 patients scheduled to undergo coronary angiography or angioplasty were enrolled and randomly assigned to a furosemide treatment or control group. All patients received supplemental hydration. Immediately after surgery, patients in the furosemide group received intravenous furosemide injection (20 mg); those in the control group received no treatment. Total fluid intake and urine output were recorded. Pre- and postsurgical changes in serum creatinine levels (SCr), glomerular filtration rate (GFR) and creatinine clearance rate (CCr) were assessed, and the incidence of CIN was also evaluated between the two groups. Logistic regression analysis was used to study risk factors for CIN. Results: General baseline conditions were similar between the two groups. Patients who received furosemide had significantly less increase in SCr and a more marked increase in GFR and CCr than those who did not. The incidence of CIN was significantly higher in the control group. Logistic regression analysis revealed that female gender and angiotensin-converting enzyme inhibitor were risk factors for CIN, whereas furosemide acted as a protective agent. Conclusions: With full hydration, small doses of furosemide can reduce CIN better than hydration alone.
  Cardiology 05/2013; 125(2):69-73.
• Article: The Effects of Ezetimibe/Simvastatin versus Simvastatin Monotherapy on Platelet and Inflammatory Biomarkers in Patients with Metabolic Syndrome.

  Michael Miller, James J Dinicolantonio, Mehmet Can, Rachel Grice, Abigail Damoulakis, Victor L Serebruany
  [show abstract] [hide abstract]
  ABSTRACT: In a randomized, double-blind, crossover study of 15 aspirin-naive patients (mean age 48.8 ± 10.2 years) with the metabolic syndrome, statin monotherapy (simvastatin 40 mg daily) was compared to combination therapy (simvastatin 40 mg and ezetimibe 10 mg daily) on biomarkers of inflammation and platelet activity. The addition of ezetimibe to simvastatin over a 4-week period was associated with reduced expression of CD141 (thrombomodulin; p = 0.02), platelet endothelial cell adhesion molecule (p < 0.0001) and CD51/61 (vitronectin receptor; p = 0.048) compared to statin monotherapy. Ezetimibe added to simvastatin improves several indices of platelet reactivity beyond statin monotherapy. However, the clinical relevance of these findings await results of the IMPROVE-IT trial (Improved Reduction of Outcomes: Vytorin Efficacy International Trial).
  Cardiology 05/2013; 125(2):74-77.
• Article: Plasma Renin and Cardiovascular Risk: What Is the Evidence for an Association?

  Massimo Volpe, Thomas Unger
  [show abstract] [hide abstract]
  ABSTRACT: Renin is a key component of the renin-angiotensin system (RAS), which plays an important role in the maintenance of blood pressure and electrolyte-volume homeostasis. RAS also plays a role in cardiovascular (CV) disease as a result of effects on inflammation and oxidative stress. There is growing evidence that plasma renin activity may be a marker of CV risk in hypertensive patients. This increase in CV risk likely reflects activation of the RAS as a whole. Patients undergoing treatment for hypertension experience a reactive increase in renin, especially if treated with diuretics, vasodilators or agents that block the RAS. There is not sufficient evidence, however, that this reactive increase in renin is intrinsically harmful for hypertensive patients in whom adequate levels of RAS blockade have been achieved. Indeed, in such patients, additional RAS blockade may not be beneficial and may even increase the risk of adverse events. Plasma renin may be an important prognostic indicator in untreated patients, and one that can be used to help in the choice of antihypertensive treatment. Currently, however, the link between plasma renin and CV risk in treated patients is inconsistent between different populations and in various clinical conditions, calling for further investigation.
  Cardiology 04/2013; 125(1):50-59.
• Article: Modulating Autophagy Improves Cardiac Function in a Rat Model of Early-Stage Dilated Cardiomyopathy.

  Kun Xie, Bo Jin, Yong Li, Xinping Luo, Jun Zhu, Duan Ma, Haiming Shi
  [show abstract] [hide abstract]
  ABSTRACT: Objectives: Previous studies reported that autophagy is activated in human dilated cardiomyopathy (DCM). It is still unknown whether modulating autophagy can improve cardiac function of the failing heart. Methods: We immunized rats with porcine cardiac myosin to set up a model of DCM. Rapamycin, a kind of mTOR inhibitor upregulating autophagy, was given to rats weeks after the immunization at low (1 mg/kg · day i.p.), intermediate (2 mg/kg · day i.p.) and high dose (4 mg/kg · day i.p.) for 2 weeks. Results: Compared to the control group (ejection fraction, EF = 81.3 ± 3.8%), the average EF decreased in both the DCM group (EF = 56.1 ± 3.3%) and the high-dose rapamycin group (EF = 55.9 ± 3.6%), but recovered in the low-/intermediate-dose rapamycin groups (EF = 64.9 ± 4.6/69.4 ± 4.4%). Phosphorylation of p70s6k and 4E-BP1 decreased and the expression of LC3BI/II increased in all rapamycin groups. Autophagic vacuoles were easily found in these groups. However, body weight was significantly reduced in the rapamycin groups. Furthermore, mortality was increased in the high-dose rapamycin group. Conclusions: Rapamycin could improve cardiac function of early-stage DCM, but the effect of rapamycin turned out to be biphasic and the effective range appeared narrow.
  Cardiology 04/2013; 125(1):60-68.
• Article: Negative Chronotropic Effects and Coronary Ischaemic Abnormalities Following Thalidomide Therapy.

  Ali Ali, Sandeep S Hothi, Andrew Thompson, Nadim Malik
  [show abstract] [hide abstract]
  ABSTRACT: The severe teratogenic side effects of thalidomide led to its well-publicized withdrawal in the 1970s, but as it is cautiously being reintroduced into clinical use, new adverse effects are being described. A 65-year-old male with multiple myeloma received chemotherapy which included cyclophosphamide, thalidomide and dexamethasone. Whilst on this treatment he experienced severe chest pain leading to an acute hospital admission complicated by significant bradycardia with sinus pauses of 7 s, necessitating temporary right ventricular pacing. Despite correction of the bradycardia with temporary pacing, he experienced further episodes of chest pain, during which an ECG (with the pacemaker briefly switched off) showed ST elevation in the inferior leads along with runs of non-sustained ventricular tachycardia. Emergency coronary angiography demonstrated unobstructed coronary arteries. Due to ST elevation in the absence of flow-limiting coronary disease his presentation was presumed to be due to intermittent coronary artery spasm. He was started on sustained-release nifedipine without any beta-blockers and further thalidomide therapy was omitted. On this pharmacological therapy, over a period of 24 months, there were no further recurrences of any cardiac symptoms. To our knowledge there have been no previous reports of coronary artery spasm associated with the use of thalidomide. The precise mechanism remains undefined, with several plausible hypothetical pathways which we discuss. We discuss various mechanisms including autonomic, autocoid and paracrine modes of action that may underlie cardiac side effects of thalidomide. We report coronary spasm in addition to bradycardia as cardiac side effects that cardiologists and oncologists need to be alert to.
  Cardiology 04/2013; 125(1):34-37.
• Article: Overexpression of MicroRNA-1 Improves the Efficacy of Mesenchymal Stem Cell Transplantation after Myocardial Infarction.

  Feng Huang, Mei-Ling Li, Zhen-Fei Fang, Xin-Qun Hu, Qi-Ming Liu, Zhen-Jiang Liu, Liang Tang, Yan-Shu Zhao, Sheng-Hua Zhou
  [show abstract] [hide abstract]
  ABSTRACT: Background: The aim of this research was to study whether transplantation of mesenchymal stem cells (MSCs) overexpressing microRNA-1 into mouse infarcted myocardium can enhance cardiac myocyte differentiation and improve cardiac function efficiently. Methods: Eight-week-old female C57BL/6 mice underwent ligation of the left coronary artery to produce models of myocardial infarction. The ligated animals were randomly divided into 4 groups (20 in each). One week later, they were intramyocardially injected at the heart infarcted zone with microRNA-1-transduced MSCs (MSC(miR-1) group), mock-vector-transduced MSCs (MSC(null) group), MSCs (MSC group) or medium (PBS group). At 4 weeks post-transplantation, transthoracic echocardiographic assessment, histological evaluation and Western blot were performed. Results: The transplanted MSCs were able to differentiate into cardiomyocytes in the infarcted zone. Cardiac function in the MSC, MSC(null) and MSC(miR-1) groups was significantly improved compared to the PBS group (p < 0.01 or p < 0.001). However, treatment of MSCs expressing microRNA-1 was more effective for cardiac repair and improved cardiac function more efficiently by enhancing cell survival and cardiac myocyte differentiation compared to the MSC group or the MSC(null) groups (p < 0.05 or p < 0.01, respectively). Conclusions: Transplantation of microRNA-1-transfected MSCs was more conducive to repair of infarct injury and improved heart function by enhancing transplanted cells survival and cardiomyogenic differentiation.
  Cardiology 04/2013; 125(1):18-30.
• Article: Potential Benefits of Ticagrelor beyond Platelet Inhibition.

  Dennis W T Nilsen
  Cardiology 04/2013; 125(1):31-33.
• Article: Epicardial Fat Thickness and Cardio-Ankle Vascular Index without Other Inflammatory Markers May Not Provide Information to Clinicians about the Systemic Inflammation.

  Sevket Balta, Sait Demirkol, Ugur Kucuk, Murat Unlu, Mustafa Dinc, Zekeriya Arslan
  Cardiology 04/2013; 125(1):13-14.
• Article: Malignant Pericardial Effusion: Still a Long Way to Ithaca?

  George Lazaros, Christodoulos Stefanadis
  Cardiology 04/2013; 125(1):15-17.
• Article: Left Ventricular Assist Devices: From the Bench to the Clinic.

  Sangjin Lee, Kiyotaka Fukamachi, Leonard Golding, Nader Moazami, Randall C Starling
  [show abstract] [hide abstract]
  ABSTRACT: The development of ventricular assist devices (VADs) over the past 5 decades as therapy for advanced heart failure (HF) has been extraordinary. Since the original VAD design by Michael DeBakey in the early 1960s, numerous devices for mechanical circulatory support have been engineered, assessed in preclinical studies, applied to human patients in large multicenter clinical trials, and now, select devices are Food and Drug Administration-approved therapy for advanced HF patients. This review highlights select examples of durable VADs from the engineering aspect of design and conception to experimental studies and clinical application underscoring the remarkable progression of such technology to now becoming the standard of care for many advanced HF patients.
  Cardiology 04/2013; 125(1):1-12.
• Article: Ticagrelor Improves Peripheral Arterial Function in Patients with a Previous Acute Coronary Syndrome.

  Kristina Torngren, Jenny Ohman, Hanna Salmi, Johan Larsson, David Erlinge
  [show abstract] [hide abstract]
  ABSTRACT: Objective: The novel P2Y12 antagonist ticagrelor inhibits adenosine diphosphate (ADP)-induced platelet aggregation more potently than clopidogrel and reduces the incidence of myocardial infarction and total death in patients with an acute coronary syndrome (ACS). Furthermore, ticagrelor inhibits adenosine reuptake and increases coronary flow reserve during adenosine infusion in man. We wanted to determine whether ticagrelor improves peripheral arterial function in patients with a previous ACS compared to patients treated with aspirin, clopidogrel, or prasugrel. Methods: 127 patients with a previous ACS (>3 months to <3 years ago) on maintenance dose of (1) no ADP blocker (n = 35); (2) clopidogrel 75 mg (n = 35); (3) prasugrel 10 mg (n = 32), or (4) ticagrelor 90 mg twice daily (n = 25) were evaluated with peripheral arterial tonometry after forearm ischemia. Results: Ticagrelor improves peripheral arterial function compared to the other groups [(1) controls 1.78 ± 0.53; (2) clopidogrel 1.78 ± 0.45; (3) prasugrel 1.64 ± 0.33, and (4) ticagrelor 2.25 ± 0.54 (means ± SD)] with a significance of p < 0.01 for ticagrelor versus no ADP blocker, p < 0.01 for ticagrelor versus clopidogrel, and p < 0.001 for ticagrelor versus prasugrel. There were fewer patients with endothelial dysfunction (<1.67 reactive hyperemia index) in the ticagrelor group (12%) compared to aspirin (51%), clopidogrel (46%), and prasugrel (53%) (p < 0.01). Conclusion: Treatment with ticagrelor improves peripheral endothelial function compared to no ADP blocker, clopidogrel, or prasugrel treatment.
  Cardiology 04/2013; 124(4):252-258.
• Article: Infantile Hypertrophic Cardiomyopathy Associated with a Novel MYL3 Mutation.

  Allison Jay, Rashmi Chikarmane, Janet Poulik, Vinod K Misra
  [show abstract] [hide abstract]
  ABSTRACT: Mutations in genes encoding cardiac sarcomeric proteins are thought to be a very rare cause of hypertrophic cardiomyopathy (HCM) in infants and young children. We report on genetic and histopathological findings in a 3-month-old infant presenting with severe progressive HCM arising from a mutation in the gene encoding the essential light chain of myosin (MYL3). The patient was found to have a novel, paternally inherited pathogenic c.530 A>G mutation in exon 5 of the MYL3 gene. His father was asymptomatic. Although, MYL3 mutations have been previously associated with adult-onset HCM, it has not been seen in infantile forms. As such, this case adds to the emerging evidence demonstrating that familial disease associated with mutations in cardiac sarcomere protein genes may have an important role in infants and children with HCM. In addition, this case highlights the marked phenotypic heterogeneity associated with sarcomeric protein mutations both within and between families.
  Cardiology 04/2013; 124(4):248-251.
• Article: Another Ace up the Sleeve.

  Axel T Kleinsasser, Karl H Lindner
  Cardiology 04/2013; 124(4):246-247.
• Article: Authors' Reply.

  Shi Chen, Jiansong Yuan, Shubin Qiao
  [show abstract] [hide abstract]
  ABSTRACT: Not Available
  Cardiology 04/2013; 124(4):260.
• Article: Increased Expression of Connective Tissue Growth Factor and Transforming Growth Factor-Beta-1 in Atrial Myocardium of Patients with Chronic Atrial Fibrillation.

  Yong Li, Zhao Jian, Zong Ying Yang, Lin Chen, Xue Feng Wang, Rui Yan Ma, Ying Bin Xiao
  [show abstract] [hide abstract]
  ABSTRACT: Objectives: This study aimed to investigate the roles of connective tissue growth factor (CTGF) and transforming growth factor-β1 (TGF-β1) in atrial fibrosis in patients with chronic atrial fibrillation. Methods: Up to 40 cases involving simple mitral valve replacement surgery were divided into 2 groups: the chronic atrial fibrillation (cAF) group (n = 28) and the sinus rhythm group (n = 12). Echocardiography was used to measure the cardiac cavity size and analyze the cardiac function. Right atrial specimens were obtained during the operation. The collagen volume fraction in the atrial specimens was examined. The mRNA and protein levels of TGF-β1, Smad3 and CTGF were also investigated. Results: Compared with the sinus rhythm group, the cAF group had higher collagen content in the right atrial tissues. The mRNA and protein levels of TGF-β1, Smad3 and CTGF were also significantly elevated in the cAF group (p < 0.05). The mRNA and protein levels of TGF-β1 and CTGF in the cAF group correlated positively with the collagen volume fraction. The positive correlation between the expression of TGF-β1 and CTGF was also demonstrated. Conclusions: CTGF is upregulated via the TGF-β1/Smad pathway in the atrial myocardium of cAF patients. Furthermore, the TGF-β1/Smad pathway may play an important role in the structural remodeling during atrial fibrosis.
  Cardiology 04/2013; 124(4):233-240.
• Article: Ghrelin and Its Relation with N-Terminal Brain Natriuretic Peptide, Endothelin-1 and Nitric Oxide in Patients with Idiopathic Pulmonary Hypertension.

  Dan Yang, Zhihong Liu, Zihe Yang
  [show abstract] [hide abstract]
  ABSTRACT: Objectives: To investigate ghrelin levels in patients with idiopathic pulmonary arterial hypertension (IPAH) and the association of ghrelin with N-terminal brain natriuretic peptide (N-BNP), endothelin-1 (ET-1) and nitric oxide (NO). Methods: Plasma ghrelin, N-BNP, ET-1 and NO were measured, and echocardiography was performed in 20 IPAH patients and in 20 control subjects matched for age, sex and body mass index. Results: Plasma ghrelin and NT-proBNP levels were significantly higher in IPAH patients compared with values in control subjects (p < 0.05). In IPAH patients, ghrelin levels correlated positively with N-BNP (r = 0.616, p = 0.004), NO (r = 0.464, p = 0.039), right ventricle diameter (RVD; r = 0.485, p = 0.030) and pulmonary arterial systolic pressure (PASP; r = 0.591, p = 0.006). N-BNP levels correlated positively with RVD (r = 0.551, p = 0.012) and ET-1 (r = 0.451, p = 0.046). Conclusions: Plasma ghrelin levels were elevated in IPAH. Increased ghrelin levels correlated positively with N-BNP, PASP, RVD and NO, and N-BNP levels correlated positively with RVD and ET-1. Pulmonary vascular pathology is a complex imbalance of opposing forces. Ghrelin may not only provide a novel prognostic biomarker for IPAH but also be a potential new therapeutic strategy.
  Cardiology 04/2013; 124(4):241-245.
• Article: Speckle Tracking Echocardiography: A Better Method for Evaluation of Left Atrial Mechanics?

  U Kucuk, H Olgun Küçük, S Demirkol, S Balta
  Cardiology 04/2013; 124(4):259.
• Article: Malignant Pericardial Effusion.

  I Burazor, M Imazio, G Markel, Y Adler
  [show abstract] [hide abstract]
  ABSTRACT: Malignant pericardial effusion is a common and serious manifestation in malignancies. The origins of the malignant process include solid tumors or hematological malignancies, while primary neoplasms of the pericardium are less common. In the oncological patient, pericardial effusion may develop by several different mechanisms, namely by direct or metastatic spread of the primary process or as a complication of antineoplastic therapies. In some cases, pericardial effusion may be the first manifestation of the disease, and that is why malignancy must be excluded in every case of an acute pericardial disease with cardiac tamponade at presentation, rapidly increasing pericardial effusion and an incessant or recurrent course. Thus, the definite differentiation of malignant pericardial effusion and rapid diagnosis are of particular therapeutic and prognostic importance. Management of these patients is multidisciplinary and requires team work, but at present there is a need for further research. An individual treatment plan should be established, taking into account cancer stage, the patient's prognosis, local availability and experience. In emergency cases with cardiac tamponade or significant effusion, initial relief can be obtained with pericardiocentesis. Despite the magnitude of this serious problem, little progress has been made in the treatment of pericardial effusion secondary to malignant disease.
  Cardiology 04/2013; 124(4):224-232.
• Article: Risk of Kidney Injury following Cardioversion for Atrial Fibrillation.

  Jacek J Preibisz
  Cardiology 04/2013; 124(4):222-223.