Hospital Chronicles (E-Journal)
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Conventional Anticoagulant Therapy
Full text linkConventional antithrombotic therapy is the mainstay of anticoagulant therapy that have been used for over 40 years in the treatment of thrombosis before newer agents become available. It includes unfractionated heparin, low-molecular-weight heparins  (LMWHs) and vitamin K antagonists. Unfractionated heparin is a glucosaminoglycan which through binding to antithrombin accelerates thrombin inhibiton. It is administered parenterally and has an immediate start of action and a variable half-life related to the dose administered. Heparin causes prolongation of the aPTT which is the assay used to monitor its anticoagulant activity although lately anti-Xa activity assay has also been used for this purpose. The main adverse event of heparin treatment is haemorrhage. Other non-haemorrhagic serious adverse events are heparin-induced thrombocytopenia and osteoporosis. Heparin can be completely and rapidly reversed by the use of protamine sulphate. LMWHs are fragments of unfractionated heparin and act via the same mechanism. LMWHs have replaced unfractionated heparin in most indications of use because their pharmacokinetic properties allow them to be administered once or twice daily without need for routine monitoring of their anticoagulant activity. However, in situations such as renal failure, obesity and pregnancy, where clearance of the drug is altered, monitoring is required and the anti-Xa activity is the recommended test. LMWHs have the same adverse events as unfractionated heparin but to a lesser extend owing to decreased binding to platelets and osteoblasts. Protamine only partially reverses their anticoagulant effect. Vitamin K antagonists were the only orally administered anticoagulant agents until recently. They act through inhibition of the reduced form of vitamin K production which is necessary for anticoagulant factors II, VII, IX, X carboxylation and activation. Their many interactions with other drugs, foods and comorbid conditions render the stability of the anticoagulant response difficult and frequent monitoring is needed. The PT test is the most common test used to monitor VKA therapy and it is expressed as INR, a standardized ratio of patient PT to normal PT. The lower and higher INR values beyond which the incidence of adverse events increases is defined as the therapeutic range. For most indications of VKAs the therapeutic range of INR must be 2,0-3,0. The most serious adverse event of VKAs is bleeding, with the rate increasing as the INR rises >5. When reversal of anticoagulant effect is needed vitamin K is administered and in major bleeding vitamin K along with prothrombin complex concentrates (PCC) or FFP is recommended.Â
Inflammatory Response and Congestive Heart Failure Following Extensive Left Atrial Ablation
Full text linkA case of a patient with persistent atrial fibrillation and normal left ventricular systolic function who developed acute heart failure symptoms after a procedure of extensive left atrial ablation is presented and possible aetiologies are being discussed
Favorable Single-Operator Experience with VasoSeal, a Vascular Closure Device with Extravascular Collagen in a Large High-Risk Cohort of Patients Undergoing Percutaneous Coronary Interventions
Full text linkBACKGROUND: Prolonged duration of manual or mechanical compression at the site of femoral artery access after sheath removal upon completion of coronary procedures followed by extended period of bed rest has significant logistical and practical problems for both patients and hospital staff. The availability of vascular closure devices (VCDs) has ushered in a new era in the routine clinical practice in the catheterization laboratory.AIM: The aim of this prospective study was to assess the effectiveness and safety of the use of the VCD VasoSeal, a collagen plug, in patients undergoing cardiac catheterization and/or percutaneous coronary intervention (PCI).PATIENTS AND METHODS: VasoSeal was employed over 2.5 years in 388 consecutive patients mostly presenting with acute coronary syndromes and subjected mainly to PCI procedures performed via transfemoral arterial access. All the patients who underwent PCI were given 7,000 IU of heparin intravenously during the procedure and had been receiving or were acutely loaded with dual antiplatelet therapy (aspirin and clopidogrel). The majority (90.7%) of patients also received a platelet glycoprotein IIb/IIIa inhibitor during and for 12-14 hours after the procedure. The sheaths were removed at the end of the procedure and hemostasis achieved with VasoSeal.RESULTS: Deployment of the VCD was successful in 99.2%. Complete hemostasis without bleeding or hematoma was obtained in 95.4% of cases (370/388). In 3 patients VasoSeal could not be or was partially deployed. The mean time required for the placement of VasoSeal was 1 min. The mean time-to-hemostasis was 3 min. The mean time-to-mobilization was 3 hours. Only one patient developed a pseudoaneurysm of the right common femoral artery; the lesion was treated with ultrasonography -guided compression. In addition, 13 small local hematomas and 2 large inguinal hematomas (one requiring blood transfusion) were recorded. In 2 cases retroperitoneal bleeding occurred, requiring blood transfusion in one of them. Local infection (cellulitis) responding to antibiotic treatment was observed in 2 patients. No patient required local surgical intervention.CONCLUSION: VasoSeal was a safe collagen closure device characterized by a high success rate of deployment and highly successful hemostasis with few manageable complications in a very high-risk patient cohort undergoing PCI under heavy anticoagulation and antiplatelet drug therapy. In these patients this vascular closure device reduced the time-to-hemostasis and time-to-mobilization and the incidence of complications
Statin-Induced Musculoskeletal Problems: Disconcerting Reports and Data
Full text linkStatins are molecules of fungal origin, which inhibit the hydroxymethylglutaryl-CoA (HMG-CoA) reductase enzyme, a key step in the sterol biosysnthesis, rendering them powerful cholesterol lowering medications contributing to significant prevention of cardiovascular disease.1 Statins are characterized by differences in bioavailability, lipo/hydrophilicity, cytochrome P-450 mediated metabolism and cellular transport mechanisms, differences that are reflected in their relative capacity in LDL-cholesterol lowering and possibly in parenchymal or muscular toxicities.2 Statin intolerance comprises, among others, musculoskeletal problems, such as statin-induced muscle and tendon disorders which are the most common cause of statin discontinuation.3-10 Musculoskeletal Problems Statin therapy has long been associated with musculoskeletal (MS) problems in approximately 10% - 25% of patients treated in real-world clinical practice, but such problems have rarely been reported in controlled clinical trials,3,4 and their incidence has thus far been underestimated.5 Studies have concentrated on creatine kinase (CK) elevations to identify myopathy. However, many patients can have normal serum CK levels despite myalgia and persistent weakness and muscle biopsy - proven myopathy. Discontinuation of statin and rechalllenge may be required to prove that it is statin-related. Several risk factors may predispose patients to statin-related MS problems, including advanced age, family history of myopathy, statin dose, and interacting medications (e.g., azole antifungals, cimetidine, fibrates, macrolide antibiotics, protease inhibitors and cyclosporine) (Table 1).5,6,8 Musculoskeletal conditions, arthropathies, injuries, and pain appear to be more common among statin users than among similar nonusers... (excerpt
Myocarditis: A Rheumatologic Perspective
Full text linkMyocarditis is an uncommon complication in patients with autoimmune rheumatic diseases. The majority of cases refer to postmortem findings. The mechanism of myocardial damage in Connective Tissue Diseases (CTDs) depends on the pathophysiology of underlying disease. Systemic inflammation, impaired microvascular circulation and vasculitis affect myocardial remodeling process, cause repeated focal ischemia resulting in hypertrophy, fibrosis of myocardium, conductive system and thus reduced contractility. Additionally, immunological abnormalities, coexisting myositis and the degree of disease activity are predictors of myocarditis progression. Clinical manifestations range from subclinical to severe forms. Early recognition is important for institution of appropriate immunomodulatory therapy
Sudden Arrhythmic Death: Family Evaluation Identifies the Cause
Full text linkA 23-year-old female professional dancer died suddenly following physical activity. Routine postmortem examination failed to establish the cause of death. No cardiac structural abnormalities were revealed. She had a history of presyncopal episodes during the last two months preceding her sudden cardiac death (SCD). Following the proband’s death, her family was referred to our department for clinical evaluation. Following informed consent, family members were evaluated with a standard protocol. All individuals underwent detailed non-invasive evaluation followed by genetic testing.The proband’s uncle was the first family member to undergo clinical investigation. He had been diagnosed with arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) almost 5 years before his niece’s SCD. The proband was positive for a plakophilin-2 (PKP2) mutation and both her father and uncle had a typical form of the ARVC/D disease. To strengthen our diagnostic assessment an immunohistochemical analysis was undertaken of a myocardial sample obtained at autopsy, which pointed towards ARVC. Thus, her death was attributed to ARVC. Probably, the mutation had been inherited from her paternal grandfather. Although he had never been clinically evaluated, and no tissue was available for genetic analysis, he had a history of SCD at the age of 72, thus, raising suspicions of cardiac diseas
Systemic Mastocytosis
Full text linkA 64-year-old man was admitted to the hematology ward due to neutropenia and thrombocytopenia. The only symptom in the month preceding his admission, was significant weight loss. Based on clinical and laboratory investigations, specifically bone marrow aspiration and biopsy, the patient was diagnosed with aggressive systemic mastocytosis (WHO 2008 ICD-0 code 9741/3)
Moderate Intake of Flavonoid-Rich Tea, Green or Black, Confers Cardiovascular Protection
Full text linkA variety of dietary supplements have been proposed for the management of hypertension and other cardiovascular diseases, but the evidence for their efficacy is meagre.1 However, over the last few years, there is growing interest in the potential benefit of tea in cardiovascular protection.2-4 Tea is the extract of Camellia sinensis, and one of the most widely enjoyed drinks.2,3 The leaves of the plant are rich in flavonoids, containing several phytochemicals including phenols and catechins, to which potent antioxidant, free radical scavenging, appetite-modifying and hypolipidemic effects have been ascribed.2-7 Long-term consumption of beverages containing catechins inhibits the formation of oxidized lipids and decreases body fat.5-9 Over 70% of flavonoids in green tea are catechins. Epigallocatechin-3-gallate (EGCG) is the cardinal (65%) catechin in green tea. In-vitro studies have shown that the epigallocatechins in green tea have angiotensin converting enzyme inhibitor properties,10 and vasodilatory actions. 11 Molecular and animal studies have demonstrated that green tea catechins enhance processes, thought to stimulate bile acid production, decrease cholesterol concentration in the hepatocytes, inhibit intestinal absorption of lipids and upregulate low-density lipoprotein (LDL) receptors in the liver, mechanisms all leading to favorable blood lipid profile.2-4,12,13 Black tea also contains small amounts of catechins. However, due to the fermentation process of black tea, its primary antioxidant polyphenols are theaflavins and thearubigins, equally effective antioxidants to catechins. 14... (excerpt
Cardiology News /Recent Literature Review / Last 2 Quarters 2014
Full text link20thAnnual Boston AF Symposium: Orlando, 8-10/1/15 HCS Working Groups Seminar: Ioannina, 2/2015ACC: San Diego, 14-16/3/15HRS: Boston, 13-16/5/15EuroPCR: Paris, 19-22/5/15Europace: Milan, 21-24/6/15ESC: London, 29/8-2/9/15AFFORD study: n-3 Polyunsaturated Fatty Acids (Fish Oil) do not Reduce Atrial Fibrillation RecurrencesIn a double-blind, randomized, placebo-controlled trial of fish oil (4 g/day, docosahexaenoic acid - DHA: eicosapentaenoic acid - EPA 1:2) vs safflower oil placebo in 337 patients with symptomatic paroxysmal or persistent AF followed for 9 ± 4 months, the primary endpoint (time to first symptomatic or asymptomatic AF recurrence lasting >30 s) occurred in 64% of patients in the fish oil arm and 63% of patients in the placebo arm (hazard ratio: 1.10; p= NS). hs-CRP and myeloperoxidase - MPO were normal at baseline and decreased to a similar degree at 6 months. The authors concluded that high-dose fish oil does not reduce AF recurrence in patients with a history of AF not receiving AA therapy, and does not reduce inflammation or oxidative stress markers in this population (Nigam A et al, J Am Coll Cardiol 2014;64:1441-1448).N.B.: Another randomized study(VITAL - VITamin D and OmegA-3 TriaL) is currently examining the effect of 1 g/d of n-3 PUFAs on AF in a much larger population (N=25,875) without cardiac disease over 5 years. RELAX-AHF: Serelaxin ReducesMainly Cardiova-scular &Sudden Deaths, Rather than Heart Failure Deaths The RELAX-AHF study showed thatIV serelaxin (recombinant human relaxin-2) compared with placebo reduced mortality at 6 months among 1,161 patients with acute heart failure (HF). In this group there were 107 deaths (9.3%): 37 (35%) from HF, 25 (23%) from sudden death, 15 (14%) from other cardiovascular (CV) causes, 19 (18%) from non-CV causes, and 11 (10%) classified as unknown. The treatment effect of serelaxin was most pronounced on other CV deaths (hazard ratio - HR: 0.29; p= 0.005) and sudden death (HR: 0.46; p= 0.065), with no effect of serelaxin treatment on HF or non-CV deaths. The authors concluded thatthe effects of serelaxin on mortality were mainly due to reduced CV causes and sudden death, without apparent effect on HF deaths (Feleker GM et al, J Am Coll Cardiol 2014;64:1591-1598). N.B.: an ongoing large phase III outcome trial (NCT01870778) will further examine serelaxin’s effect on mortality... (excerpt
Adverse Cardiovascular Events with Nonsteroidal Anti-inflammatory Agents
Full text linkThe extensive use of nonsteroidal anti-inflammatory drugs (NSAIDs), both nonselective and cyclooxygenase- 2–specific inhibitors, for the relief of acute and chronic musculoskeletal pain, in addition to gastrointestinal toxicity, confers serious cardiovascular toxicity that affects the overall risk/benefit ratio of this commonly employed therapy. A plethora of studies have provided convincing evidence for a high risk of adverse cardiovascular events associated with NSAIDs related to a number of risk factors, which are herein briefly reviewed and an algorithm is suggested for their safer use