Signs Of Acute Heart Failure Research Articles

Takotsubo cardiomyopathy in association with endogenous and exogenous thyrotoxicosis

### Case 1 A 79-year-old woman from Sri Lanka, with a history of hyperthyroidism, presented with chest pain and breathlessness following an episode of extreme anxiety after missing her connecting flight. She had been unable to take carbimazole during the preceding 3 months due to local shortages. Examination revealed signs of acute heart failure, with an electrocardiogram (ECG) showing anterior T-wave inversion, a 12-h cardiac Troponin I of 4.1 ng/ml and thyroid function tests demonstrating thyrotoxicosis (free thyroxine [fT4] 40.4 pmol/l, thyroid-stimulating hormone [TSH] 0.04 mU/l). Coronary angiography showed only minor disease in the left anterior descending and circumflex arteries. Ventriculography revealed classical apical ballooning and left ventricular dysfunction. Cardiovascular magnetic resonance (CMR) imaging on Day 3 confirmed this finding on cine imaging and without evidence of delayed gadolinium hyperenhancement (Figure 1). Her symptoms resolved within 4 …

Lethal thyroid storm after uncontrolled intake of liothyronine in order to lose weight

Thyroid hormones are sometimes used for purposes for which they are not approved. Reasons for off-label use can be overweight, prevailing depressive mood, or various somatic symptoms. Information about the intake of thyroid hormones in order to lose weight can be easily obtained from inappropriate/nonmedical websites. The objective of this case report is to describe the first case of a lethal abuse of liothyronine. The case was a 29-year-old male (BMI 32) without relevant illnesses. An autopsy was performed and followed by histological, toxicological, and clinical chemistry examinations. The autopsy revealed no relevant pathology. Histology showed multiple areas of focal cell necrosis in the myocardium and signs of acute heart failure including severe edema of the lungs; the follicles of the thyroid gland were markedly plump. Postmortem laboratory results indicated lethal liothyronine intoxication. Despite prevailing opinion, uncontrolled intake of liothyronine can cause lethal thyroid storm in a euthyroid patient without manifested cardiac illnesses.

The influence of beta-blockade on the hemodynamic effects of levosimendan in elderly (>= 70 years) patients with acutely decompensated systolic heart failure

The purpose of this study was to evaluate the influence of chronic beta-blockade on the hemodynamic parameters in elderly (>or= 70 years) patients with acutely decompensated systolic heart failure treated with levosimendan. Eighteen patients with acutely decompensated systolic heart failure (8 on chronic beta-blockade) were included in this study. Inclusion criteria were symptoms and signs of acute heart failure in the presence of: a) left ventricular ejection fraction < 0.35; b) cardiac index < 2.5 l/min/m2, c) pulmonary capillary wedge pressure > 15 mmHg; and d) systolic blood pressure between 90 and 110 mmHg. After completion of baseline hemodynamic measurements, a levosimendan intravenous infusion was started (initial loading dose given as an infusion of 24 microg/kg over 10 minutes, followed by a continuous infusion of 0.1 microg/kg/min for 24 hours). At the end of levosimendan infusion hemodynamic measurements were repeated. Demographic characteristics as well as baseline systolic and diastolic blood pressure were not significantly different between patients not receiving beta-blockers (Group A) and those under beta-blockade (Group B), whereas heart rate was significantly lower in the latter. Treatment with levosimendan was associated with an increase in the cardiac index and a decrease in wedge pressure in both groups (Group A: 43.8% and 33%; p < 0.001 vs. baseline; Group B: 17.72% and 17.5%, p < 0.001 vs. baseline, respectively). Peripheral and pulmonary resistance significantly decreased in both groups (31% vs. 15%, p < 0.001 and 44.5% vs. 25%, p < 0.001, respectively). Thus, the beneficial hemodynamic effects of levosimendan are maintained in elderly patients with acute decompensated systolic heart failure treated with beta-blockers.

Dobutamine in acute myocardial infarction: should we use it for reduction of pulmonary hypertension and pulmonary capillary wedge pressure in acute myocardial infarction?

Enthusiasm for application of dobutamine has retreated after the introduction to clinical practice of new medications such as levosimendan. Such treatment, however, is rather expensive as well as remote outcomes still being under discussion. Owing to this, dobutamine still has an appropriate place in the treatment of patients with complicated acute myocardial infarction (AMI) where signs of acute heart failure and pulmonary hypertension should be treated immediately. The study objective was to evaluate the hemodynamic effect of dobutamine using the pulmonary artery catheterization technique in patients with AMI complicated by cardiogenic shock and pulmonary hypertension.

Pericardial Effusion With Beginning Cardiac Tamponade Caused by a Spontaneous Coronary Artery Rupture

A 65-year-old man was admitted to his local hospital with troponin-positive acute coronary syndrome. The patient developed signs of acute heart failure and was immediately transferred to our center. Echocardiography demonstrated a pericardial mass (8×5 cm) with compression of the right atrium (Figure 1 and online-only Data Supplement Movie I) and a reduced contractility of the posterior left ventricular wall. Magnetic resonance imaging demonstrated a pericardial hematoma that was incompressible, not vascularized, and impinging on the right atrium (Figure 2 and online-only Data Supplement Movie II). Figure 1. Echocardiographic 4-chamber view with …

Acute heart failure and near-syncope associated with giant left atrial ball thrombus occluding left ventricular inflow tract

A 70-year-old female patient was admitted to our department with symptoms and signs of acute heart failure and near syncope. After hospitalization, both transthoracic echocardiography (TTE) and subsequent transesophageal echocardiography (TEE) demonstrated a giant (4.9 x 3.9 cm) mobile, irregular, bright left atrial mass consistent with left atrial ball thrombus (LABT). The mass was found to occlude the left ventricular inflow tract (LVIT) above the mitral orifice (supravalvular) in the presence of normal mitral leaflets. After emergent surgical excision, the pathology of the left atrial mass was found to be consistent with thrombus. The case presented here suffered acute diastolic heart failure and near-syncope due to obstruction of the LVIT above the mitral orifice by a giant LABT.

Prise en charge thérapeutique de l'insuffisance cardiaque et de la dysfonction ventriculaire gauche post-infarctus du myocarde dans les unités de soins intensifs en cardiologie française

Objective To evaluate the therapeutic management of cardiac failure after myocardial infarction (MI) in French intensive cardiac care units (USIC) in 2005. Method French cross-sectional observational study conducted in USIC of University Hospital Centres (CHU), General Hospital Centres (CHG), and private clinics. Included patients were hospitalized for MI, with a systolic ejection fraction ≤ 40% and “having” or “having had” signs of acute heart failure during the hospitalization or diabetes. Results Overall, 59 sites, including 10 CHU (16.9%), 37 CHG (62.7%), and 12 private clinics (20.3%) included 447 patients. The majority of patients were male (64.9%), ≥ 70 years (62.7%), hypertensive (53.5%) and diabetic (40.8%). They presented a class II (22.3%), class III (29.5%) and class IV (38.9%) cardiac failure severity according to NYHA classification and 20.4% had a creatinine clearance < 30ml/min. The most prescribed treatments were statines (75.4%), IEC (73.6%), diuretics (71.8%) and betablockers (66.7%). The least prescribed were aldosterone antagonist (16.3%) and calcium channel blockers (6.5%). Treatments were prescribed according to age, degree of cardiac failure and renal function of the patient. Conclusion The present observational study shows improved compliance with European and international guidelines, as regards the medications prescribed at hospital discharge after myocardial infarctions complicated with left ventricular dysfunction. Unfortunately, recommended medications remained less often prescribed in the patients with the most severe characteristics.

AT1 receptor antagonists—beyond blood pressure control: possible place in heart failure treatment

The renin-angiotensin system (RAS) plays an important role in heart failure, and renin angiotensin aldosterone blockade has been shown to be of benefit in its treatment. The effectiveness of angiotensin...

Schwangerschaftskardiomyopathie in der 22. SSW - Cardiomyopathy of Pregnancy at 22 Weeks' Gestation: A Case Report -

Wir berichten über eine 30-jährige Patientin (G IV, P I), die in der 21 + 6 SSW mit Zeichen einer akuten Herzinsuffizienz bei Schwangerschaftskardiomyopathie stationär aufgenommen wurde. Andere Ursachen einer Herzinsuffizienz konnten ausgeschlossen werden. Trotz Ausschöpfung der medikamentösen Therapie blieb die Behandlung der Herzinsuffizienz ohne Erfolg. Nach sorgfältiger Beratung der Patientin durch den Geburtshelfer und den Kardiologen entschloss sie sich zur Beendigung der Schwangerschaft in der 24 + 5 SSW. Postpartal verbesserten sich ihre Beschwerden deutlich. Die echokardiographische Kontrolle vor Entlassung ergab jedoch eine persistierende linksventrikuläre Dysfunktion. Auch nach 6 Monaten zeigte sich in der invasiven Herzdiagnostik keine Verbesserung der linksventrikulären Funktion. In der Myokardbiopsie sah man das typische Bild einer dilatativen Kardiomyopathie ohne Zeichen einer Myokarditis.

Solving the Microgram/Kilogram Puzzle

ou work as a critical care nurse in a university teaching facility, and this evening you're moonlighting at a local community hospital. During your CCU shift here, Alexander Schmitt, age 43 and weighing 220 lbs. (100 kg), is admitted from the ED with a diagnosis of acute anterior wall myocardial infarction. In the ED, his EKG showed acute S-T elevation in leads V2 through V4. The ED nurse had initiated streptokinase by physician order; a heparin bolus of 5,000 units, a heparin drip at 1,000 units/hr, and a nitroglycerin drip at 10 mcg/min were ordered as well. Mr. Schmitt also received one baby aspirin and 15 mg metoprolol. You assess his vital signs: BP, 101/58 mmHg; P, 102 beats per minute; R, 20 per minute; and T, 98.4oE Mr. Schmitt rates his chest pain at about 5 or 6 on a 1-to-10 scale. You note that the nitroglycerin drip (50 mg/250 cc) is infusing at 50 cc/hr, and the heparin drip (25,000 units/250 cc) at 10 cc/hr. You're familiar with different concentrations of nitroglycerin in your own hospital, where the drug is available in the manufacturer's premixed bags. You realize that here you'll need to check the calculations for the nitroglycerin dose and rate. Per the physician's orders, you administer morphine sulfate 2 mg Iv to relieve Mr. Schmitt's pain. Moments later, he rates his chest pain at only 1 or 2. At the nurses' station, you check the order and begin calculating the dose and rate of nitroglycerin. Within minutes, Mr. Schmitt calls your name; something's wrong, he says. His vital signs have changed: Blood pressure is 92/54 mmHg; pulse is 110 beats per minute; respirations are 22 per minute. You auscultate his heart and lungs and hear an S3 and crackles in all lung fields. Mr. Schmitt stops talking to you mid-sentence-his level of consciousness is decreasing. Blood pressure has now dropped to 88/40 mmHg; pulse has risen to 120 beats per minute; respirations are 24 per minute. You immediately stop the nitroglycerin drip and call to the physician in charge. She orders a dopamine drip (400 mg/250 cc) at 5 mcg/kg/min, or 19 cc/hr. Mr. Schmitt's vital signs begin to improve, and the physician orders resumption of the nitroglycerin drip at 10 mcg/min (3 cc/hr). Your immediate discontinuation of nitroglycerin probably saved Mr. Schmitt's life. He showed signs of acute heart failure, and his MI may have been extending. Inaccurate calculation of the drip rate-50 cc/hr was far too high for this concentration-resulted in a nitroglycerin overdose, precipitating a rapid fall in blood pressure and acute cardiac symptoms. Vasoactive medications are usually administered as micrograms per kilogram of body weight per minute. It's important to carefully calculate the dosage at the beginning of a shift and to check any drips already infusing.