[Iron deficiency in heart failure: beyond the anemia.] / Iron deficiency nello scompenso cardiaco: oltre l'anemia.

Iron deficiency in heart failure is a frequent condition and may be a prerequisite for the development of anemia but not necessarily the two conditions coexist. Iron deficiency in itself independently of the presence of anemia, determines a series of alterations of the cellular processes of our body related to the production of energy in the form of ATP, cell proliferation and DNA synthesis. The causes of iron deficiency are several and among the various, the inflammatory state present in chronic heart failure, combined with the absorption deficit seems to play a predominant role. This review aims to cover all the main aspects related to iron deficiency in patients with heart failure starting from aetiology up to the therapeutic implications. In particular, the different causes and the pathophysiological mechanisms that underlie the iron deficiency will be examined, describing what are the consequences on the alterations on the biochemical processes in terms of absorption, transport and use of iron by target cells with particular regard to muscle cells and Erythropoietic line. The meaning, the role and the importance in clinical practice of the different laboratory tests that dose the iron (Ferritin, Serum Iron, Transferrin and Transferrin saturation or TSAT) that allow to identify the presence of absolute or relative iron deficiency will also be underlined. Literature data related to the consequences of iron deficiency and to the alterations concerning its transport on the symptoms and functional capacity of patients with heart failure will be reported as well as their impact on prognosis. A second part of the paper will address the main aspects related to iron therapy. We will discuss the administration of iron per os with regard to the different drugs, to the processes of absorption and to the use of different pharmaceutical formulations with their associated side effects. The scientific evidences on parenteral formulations and in particular on the use of Fe-carboxymaltose will be reported. Finally, we will discuss the role of erythropoietin in the context of heart failure.

Early and personalized ambulatory follow-up to tailor furosemide and fluid intake according to congestion in post-discharge heart failure.

Congestive heart failure (CHF) worsening is a worldwide cause of rehospitalization and mortality, specially during the early period after hospitalization. Fluid accumulation plays a key role in the pathophysiology of both acute heart decompensation and disease progression. The effective use of drugs to maintain restored clinical stabilization in recently discharged patients is a difficult task, and it relies on matching the most appropriately tailored therapy to specific clinical profiles. However, no successful treatment has been shown to reduce post-discharge readmission. We evaluated in a case-control study the effectiveness of an early and personalized congestion-guided ambulatory program on medium-term (6 months) compensation in recently discharged CHF patients. Group A (22 patients) underwent a post-discharge close follow-up consisting of: an early clinic visit within 10 days; a second visit within 10 days after the first; and the other visits at month 1, 2, 3 after discharge. Controls (Group B, 21 patients) underwent a conventional ambulatory follow-up only at month 1, 2, 3 after discharge. The ambulatory approach in both groups was based on the monitoring of signs/symptoms of congestion and body weight, body hydration estimation by using bioelectrical impedance analysis (BIA) and laboratory data. This assessment was finalized to tailor furosemide and daily fluid intake at each visit to eliminate clinical or instrumental evidence of persistent congestion relieving the signs and symptoms. At 6 months, Group A was associated with a better clinical compensation (improved hydration state, lower BNP levels and congestion score), an improved quality of life, and reduced re-hospitalizations. We conclude that in CHF the early and personalized ambulatory follow-up based on congestion-guided treatment is effective to optimize management and maintain clinical stability in the post-discharge period.

Large hiatal hernia at chest radiography in a woman with cardiorespiratory symptoms.

Hiatal hernia (HH) is a frequent entity. Rarely, it may exert a wide spectrum of clinical presentations mimicking acute cardiovascular events such as angina-like chest pain until manifestations of cardiac compression that can include postprandial syncope, exercise intolerance, respiratory function, recurrent acute heart failure, and hemodynamic collapse. A 69-year-old woman presented to the emergency department complaining of fatigue on exertion, cough, and episodes of restrosternal pain with less than 1 hour of duration. Her medical history only included some episodes of bronchitis and no history of hypertension. The 12-lead electrocardiogram demonstrated sinus rhythm with right bundle-branch block. Laboratory tests, including cardiac troponin I, were within normal reference values. Chest radiography showed no significant pulmonary alterations and revealed in mediastinum a huge abnormal shadow overlapping the right heart compatible with a gastric bubble.The gastroscopy confirmed a large HH. A 2-dimensional transthoracic echocardiogram, using all standard and modified apical and parasternal views, revealed an echolucent mass, compatible with HH, compressing the right atrium. Also, it showed an altered left ventricular relaxation and a mild increase of pulmonary artery pressure (35 mm Hg). Spirometry showed a mild obstruction of the small airways, whereas coronary angiography showed normal coronary arteries. We concluded that the patient's symptomatology was related to the compressive effects of the large hiatal ernia, a neglected cause of cardiorespiratory symptoms. The surgical repair of HH was indicated.

Sudden severe abdominal pain after a single low dose of paracetamol/codein in a cholecystectomized patient: learning from a case report.

We report the case of an elderly patient with diastolic heart failure and renal insufficiency admitted to hospital as he complained of having a history of hypogastric pain and dysuria without fever due to renal lithiasis and urinary infection. Because the pain was persistence, and considering the presence of renal dysfunction, it was administered a single low dose of paracetamol/codein (500/30 mg). After about 1 hour of the administration, he suddenly complained of the onset of a lancinating epigastric pain radiating to the whole abdomen and retrosternum accompanied by nausea. The electrocardiogram (EKG) was negative for myocardial infarction and computed tomography excluded aortic dissection and other causes of acute abdomen. Laboratory tests showed instead liver and pancreatic damage. The symptomatology was relieved 3 hours later of the onset after antispastic treatment with anticholinergics (floroglucine). The likely underlying pathophysiological mechanism is the codein-induced spasm of the sphincter of Oddi combined with dysfunction of the same sphincter and reduced bile storage capacity related to a previous cholecystectomy. When a similar event does not regress, it may lead to more severe conditions such as acute pancreatitis. Since codein is a widely used drug, this report may suggest cholecystectomy as a contraindication during administration for the risk of occurrence of these complications.

One-year renal and cardiac effects of bisoprolol versus losartan in recently diagnosed hypertensive patients: a randomized, double-blind study.

BACKGROUND AND OBJECTIVES: Hypertension is a significant cause of chronic renal injury and its effective treatment is capable of reducing the rate of renal failure. beta-Adrenoceptor antagonists (beta-blockers) have been reported to induce a deterioration in renal function, while several data have indicated a renoprotective effect of treatment with the angiotensin II type 1 receptor antagonist losartan. Previous studies of the interaction between the selective beta(1)-blocker bisoprolol and kidney function were performed only for short- and medium-term periods. The aim of this study was to compare the antihypertensive efficacy and renal and cardiac haemodynamic effects of bisoprolol with those of losartan over a 1-year time period in patients with essential hypertension. METHODS: Seventy-two patients (40 males) with recently diagnosed uncomplicated (European Society of Hypertension [ESH] criteria stage 1-2) hypertension (mean +/- SD age 52 +/- 12 years) were enrolled in the study. After a run-in period of 14 days on placebo, the patients were randomized in a double-blind, prospective study to receive either bisoprolol 5 mg or losartan 50 mg, administered once daily for 1 year. At recruitment and 12 months after treatment, cardiac output and renal haemodynamics and function were evaluated by echocardiography and radionuclide studies, respectively. RESULTS: There were no significant differences in baseline clinical data, including glomerular filtration rate and blood pressure, between the two treatment groups. At 1 year, blood pressure had decreased significantly (p < 0.001) with both treatments, and heart rate was reduced only in the group taking bisoprolol. The long-term effects on renal haemodynamics and cardiac function were similar with both drugs, the only change being a significant reduction in the filtration fraction for each group. CONCLUSIONS: These data suggest that both bisoprolol and losartan are effective agents for the treatment of patients with recently diagnosed ESH stage 1-2 hypertension. Over a 1-year period, both agents maintained good renal and cardiac performance and haemodynamics.

Transmural coronary inflammation triggers simultaneous multivessel rupture of unstable plaques.

The authors describe a case of sudden cardiac death caused by the simultaneous multivessel rupture of unstable atherosclerotic plaques, triggered by a transmural inflammatory process (coronaritis). Male subject, 44 years old, apparently in good health until 1 hour before death, when he complained of worsening dyspnea. At autopsy, it was found that the heart weighed 486 g. Evaluation of the coronary arteries revealed the presence of atherosclerotic plaques resulting in a lumen critical stenosis of the left anterior descending artery (LAD), right coronary artery (RCA) and left circumflex artery, and acute occlusive thrombosis of the LAD and RCA. Transverse sections of the ventricular mass highlighted the presence of eccentric hypertrophy of the left ventricle associated with myocardiosclerosis of the posterior interventricular septum and of the posterior wall of the left ventricle. Histology revealed the presence of a coagulative myocytolysis ascribable to the free walls of the left ventricle, and a focus of lymphocytic-active myocarditis. All coronary arteries were sites of intima fibroatheromatous plaques complicated by rupture and thrombosis within the RCA and LAD and by a transmural infiltrate consisting of macrophages and T-lymphocytes associated with consensual medionecrosis and perineuritis. In conclusion, the present case report confirms the hypothesis that inflammation plays a key role in the onset of acute coronary syndromes as it promotes the formation of an unstable plaque as well as its rupture.