Heart failure case study

Colombo, M. G., Ciofini, E., Paradossi, U., Bevilacqua, S., and Biagini, A. (2006) ET-1 Lysl98Asn and ET(A) receptor H323H polymorphisms in heart failure. A case-control study. Cardiology. 105, 246-252. 

Case Study Congestive Heart Failure with Complications... 

The significance of ammonia in clinical disease was broadened markedly when it was discovered that ammonia poisoning might be the mechanism of the cerebral symptoms associated with chronic heart failure. It has been known for a long time that the mental symptoms associated with heart failure could not be correlated with the oxygen supply to the brain, which remains, in most cases, adequate. The work of A. N. Bessman (B4) demonstrated that the ammonia content of the blood was elevated in heart failure, probably due to the chronic passive congestion of the liver which prevented the liver from removing the normally formed ammonia from the portal system. When the blood ammonia fell, the mental symptoms of heart failure were relieved. This has been confirmed by Calkins and Delph (Cl), who studied twenty-six cases of heart failure and found the blood ammonia to be elevated only in the two patients who had mental symptoms. 

Case study level Ma - Heart failure - see page 25... 

The authors of a study of the use of MRI scans to assess the subclinical effects of the anthracyclines concluded that increased MRI enhancement equal to or greater than 5 on day 3 compared with the baseline predicted significant reduction in ejection fraction at day 28 (32). In 1000 patients given doxorubicin chemotherapy and irradiation there were six cases of congestive heart failure and three cases of myocardial infarction there was a cumulative cardiac mortality of 0.4% in all anthracycUne-exposed patients (33). 

In the Randomized Aldactone Evaluation Study (RALES) in 1663 patients with New York Heart Association (NYHA) class III (70%) or IV (30%) symptoms and an ejection fraction less than 35%, the addition of spironolactone 25 mg/day to conventional treatment (an ACE inhibitor, a loop diuretic, in most cases digoxin, and in 11% a beta-blocker) for an average of 24 months lowered the risk of all-cause mortality by 30% (from 46% to 35%), death from progressive heart failure, and sudden death (28). There were similar reductions in hospital admissions for worsening heart failure and for all cardiac causes. The magnitude of the overall effect was similar and additional to the proven benefit from ACE inhibition in severe heart failure. 

In the DIAMOND study in congestive heart failure, there were 25 cases of torsade de pointes in the dofetilide... 

The use of a lower dose of enoximone in 105 patients with heart failure (New York Heart Association classes 2 or 3) has been studied over 12 weeks (12). Enoximone 25-50 mg tds improved exercise capacity and reduced dyspnea. There was no evidence of a dysrhythmic effect. The rates of adverse events were similar with enoximone and placebo, and there were fewer cases of dizziness, vertigo, or hypotension in those who took enoximone. There were two deaths in the 70 patients who took enoximone compared with four of the 35 who took placebo. However, this small short-term study does not rule out the possibility that even this small dose of enoximone can cause increased mortality during long-term administration or in patients with more severe cardiac failure. 

In 910 patients toxicity was life-threatening in 0.55% (41). A combination of cisplatin, fluorouracil, and eto-poside given for advanced non-small cell cancer of the lung caused only the expected amount of hematological toxicity, but was associated with a higher than expected incidence of cardiac, pulmonary, and cerebrovascular toxicity, including two myocardial infarctions, two cases of congestive heart failure, one pulmonary embolus, and one cerebrovascular accident in a study of 35 patients (42). 

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