ABSTRACT
Complications of any mechanical prosthesis include thrombus or pannus formation. In our case report we demonstrate that prosthetic aortic valve regurgitation due to pannus formation may be intermittent and non-cyclic in pattern and therefore not obvious at the time of original clinical examination. Under these conditions and as transesophageal echocardiography cannot be repeated promptly, transthoracic 2-D and Doppler echocardiography should be available at any time when symptoms occur and present the method of choice for acute patient evaluation. Thrombolysis seems to be the first treatment of choice in case of thrombus formation and re-do surgery in case of pannus formation.
Subject(s)
Aortic Valve Insufficiency/diagnosis , Aortic Valve Insufficiency/etiology , Heart Valve Prosthesis/adverse effects , Acute Disease , Adult , Aortic Valve Insufficiency/surgery , Aortic Valve Stenosis/surgery , Coronary Angiography , Echocardiography, Transesophageal , Electrocardiography , Fluoroscopy , Humans , Male , Prosthesis FailureABSTRACT
OBJECTIVE: The prevention of contrast-mediated nephropathy (CMN), which accounts for considerable morbidity and mortality, remains a vexing problem. Contrast induced renal vasoconstriction is believed to play a pivotal role in the CMN mechanism. The aim of this pilot study was to examine the safety and efficacy of two doses of the prostacyclin analogue iloprost in preventing CMN in high-risk patients undergoing a coronary procedure. METHODS: Forty-five patients undergoing coronary angiography and/or intervention who had a serum creatinine concentration >or=1.4 mg/dL were randomized to receive iloprost at 1 or 2 ng/kg/min or placebo, beginning 30-90 minutes before and terminating 4 hours after the procedure. CMN was defined by an absolute increase of serum creatinine >or=0.5 mg/dL or a relative increase of >or=25% measured 2 to 5 days after the procedure. Study drug infusion was discontinued in 2 patients in the low-dose iloprost group due to flush/nausea and in 5 patients in the high-dose group due to severe hypotension. RESULTS: The mean creatinine concentration change in the placebo group (0.02 mg/dL) was unfavorable compared to that in the low-dose iloprost group (-0.11 mg/dL; p=0.08) and high-dose iloprost group (-0.23 mg/dL; p=0.048). The difference between the absolute changes in creatinine clearance was favorable compared to placebo for both the low (mean difference 6.1 mL/min, 95%CI -0.5 to 12.8 mL/min, p=0.07) and the high-dose iloprost group (11.8 mL/min, 95%CI 4.7 to 18.8 mL/min, p=0.002). Three cases of CMN were recorded; all in the placebo group (p=0.032). CONCLUSIONS: The results of this pilot study suggest that prophylactic administration of iloprost may effectively prevent CMN, but higher dosages are connected with substantial tolerability issues.
Subject(s)
Contrast Media/adverse effects , Coronary Angiography , Iloprost/therapeutic use , Kidney Diseases/prevention & control , Vasodilator Agents/therapeutic use , Aged , Creatinine/blood , Female , Humans , Kidney Diseases/etiology , Male , Pilot Projects , Risk FactorsABSTRACT
We examined clinical outcomes associated with non-randomised digoxin therapy in a postmyocardial infarction population with clinical heart failure (AIRE study). Our results raise concern about the safety of digoxin in this population.
Subject(s)
Cardiotonic Agents/adverse effects , Digoxin/adverse effects , Heart Failure/drug therapy , Myocardial Infarction/drug therapy , Adult , Cardiotonic Agents/therapeutic use , Digoxin/therapeutic use , Female , Follow-Up Studies , Heart Failure/mortality , Humans , Male , Middle Aged , Myocardial Infarction/mortality , Product Surveillance, Postmarketing , Tachycardia, Ventricular/chemically induced , Tachycardia, Ventricular/mortality , Treatment OutcomeABSTRACT
BACKGROUND: QT interval dispersion is a marker of inhomogeneous ventricular repolarization, and therefore has the potential to predict re-entry arrhythmias. Following acute myocardial infarction, increased QT dispersion has been associated with a higher risk of ventricular arrhythmias. However, whether or not QT dispersion predicts prognosis post-acute myocardial infarction is not clear. We addressed this issue by analysing the AIREX study registry. METHODS: AIREX was a follow-up study of 603 post-acute myocardial infarction patients who exhibited clinical signs of heart failure and were randomly allocated to ramipril or placebo. An interpretable 12-lead ECG obtained between day 0 and day 9 after the index infarction (median time 2 days) was available in 501 patients. We examined whether QT dispersion was a predictor of all-cause mortality in the AIREX study registry (mean follow-up 6 years). RESULTS: QT dispersion measurements were significantly increased in patients who subsequently died (QT dispersion: 92.0 +/- 38.5 ms vs 82.7 +/- 34.3 ins. P=0.005; rate corrected QT dispersion: 105.7 +/- 42.7 ms vs 93.1 +/- 35.9 ms, P<0.001). Univariate analysis showed that QT dispersion as a predictor of all-cause mortality risk (QT dispersion: hazard ratio per l0 ms 1.05, [95% CI 1.02 to 1.09]. P= 0.004; rate corrected QT dispersion: 1-07 [1.03 to 1.10], P<0.001): an increase of 10 ms added a 5-7%, relative risk of death. QT dispersion remained an independent predictor of all-cause mortality risk on multivariate analysis (QT dispersion: 1.05 [1.01 to 1.09], P=0.027; rate corrected QT dispersion: 1.05 [1.01 to 1.09]. P=0.022). CONCLUSION: QT dispersion. measured from Li routine 12-lead ECG following acute myocardial infarction complicated by heart failure provides independent information regarding the probability of long-term survival. However. the low sensitivity of this electrocardiographic marker limits its usefulness for risk stratification if used in isolation.
Subject(s)
Arrhythmias, Cardiac/etiology , Arrhythmias, Cardiac/mortality , Electrocardiography , Heart Failure/complications , Heart Failure/mortality , Myocardial Infarction/complications , Myocardial Infarction/mortality , Aged , Arrhythmias, Cardiac/physiopathology , Chi-Square Distribution , Female , Follow-Up Studies , Heart Failure/physiopathology , Humans , Male , Middle Aged , Multivariate Analysis , Myocardial Infarction/physiopathology , Predictive Value of Tests , Prognosis , Proportional Hazards Models , Registries , Sensitivity and Specificity , Survival RateABSTRACT
BACKGROUND: After acute myocardial infarction (AMI), patients with a history of arterial hypertension (AH) have a worse prognosis than normotensives. Whether this adverse risk is beneficially modulated by treatment with angiotensin-converting enzyme (ACE) inhibitors is unknown. We evaluated the prognostic value of antecedent hypertension in post-AMI patients given ACE inhibitor therapy. METHODS: We analysed retrospectively data from the AIRE study (randomised, placebo-controlled trial of ramipril in 2006 post-AMI patients with clinical heart failure). A history of AH was present in 28% of the patients. We examined the prognostic value of antecedent hypertension separately among placebo and ramipril treated patients and also the effect of ramipril on clinical outcomes according to whether or not a history of AH was present. RESULTS: Antecedent hypertension was a significant indicator of adverse prognosis in the placebo (P) treated patients (Hazard Ratio 1.49, 95% Confidence Intervals 1.13 to 1.97, P = 0.005) but not in the ramipril (R) treated patients (1.17, 0.84 to 1.61, P = 0.34). A similar pattern was observed for the risks of sudden death (P: 1.75, 1.21 to 2.54, P = 0.003; R: 1.34, 0.86 to 2.07, P = 0.18) and severe/resistant heart failure (P: 1.48, 1.08 to 2.03, P = 0.014; R: 1.18, 0.83 to 1.68, P = 0.37). Treatment with ramipril reduced the all-cause mortality risk in both hypertensive (0.63, 0.44 to 0.89, P = 0.009) and normotensive patients (0.78, 0.61 to 0.99, P = 0.041). CONCLUSION: Antecedent hypertension is not a significant prognosticator in patients with AMI and clinical heart failure given ACE inhibitor therapy.
Subject(s)
Hypertension/complications , Hypertension/drug therapy , Medical Records , Myocardial Infarction/complications , Ramipril/therapeutic use , Aged , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Antihypertensive Agents/therapeutic use , Cardiac Output, Low/etiology , Cardiac Output, Low/mortality , Cohort Studies , Death, Sudden, Cardiac/etiology , Female , Humans , Male , Middle Aged , Multivariate Analysis , Placebos , Prognosis , Proportional Hazards Models , Retrospective StudiesABSTRACT
In a cohort of 67 patients from the Acute Infarction Ramipril Efficacy study, we showed that ramipril therapy was associated with a significant reduction in QT dispersion over a 2-month period after acute myocardial infarction. This reduction of ventricular repolarization inhomogeneity indicates an antiarrhythmic effect and may be an important additional mechanism for the reduced all-cause mortality and sudden death incidence achieved with angiotensin-converting enzyme inhibition after acute myocardial infarction.
Subject(s)
Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Electrocardiography/drug effects , Myocardial Infarction/drug therapy , Ramipril/therapeutic use , Female , Heart Failure/etiology , Humans , Male , Middle Aged , Myocardial Infarction/complications , Myocardial Infarction/physiopathology , Single-Blind MethodABSTRACT
OBJECTIVES: To examine clinical outcomes associated with optional beta blockade in a population of patients with evidence of heart failure after myocardial infarction. DESIGN AND PATIENTS: Data from the acute infarction ramipril efficacy (AIRE) study were analysed retrospectively. At baseline 22.3% of the patients were receiving a beta blocker. To minimise confounding, beta blocker and diuretic treatments, presence of clinical signs of heart failure, left ventricular ejection fraction, and 16 other baseline clinical variables were simultaneously entered in a multivariate Cox regression model. In addition, the same analysis was repeated separately within a high and a low risk group of patients, as defined according to the need for diuretic treatment. RESULTS: beta Blocker treatment was an independent predictor of reduced risk of total mortality (hazard ratio 0.66, 95% confidence interval (CI) 0. 48 to 0.90) and progression to severe heart failure (0.58, 95% CI 0.40 to 0.83) for the entire study population. There were similar findings in high risk patients requiring diuretics (0.59, 95% CI 0.40 to 0.86; and 0.58, 95% CI 0.38 to 0.89). CONCLUSIONS: beta Blocker treatment is associated with improved outcomes in patients with clinical evidence of mild to moderate heart failure after myocardial infarction. Most importantly, high risk patients with persistent heart failure appear to benefit at least as much as lower risk patients with transient heart failure.
Subject(s)
Adrenergic beta-Antagonists/therapeutic use , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Heart Failure/drug therapy , Myocardial Infarction/complications , Ramipril/therapeutic use , Aged , Diuretics/therapeutic use , Double-Blind Method , Drug Therapy, Combination , Female , Heart Failure/etiology , Heart Failure/mortality , Humans , Male , Middle Aged , Myocardial Infarction/mortality , Regression Analysis , Retrospective Studies , Risk Factors , Treatment OutcomeABSTRACT
It is now clear that angiotensin-converting enzyme (ACE) inhibitor treatment after myocardial infarction (MI) reduces mortality and morbidity. However, the benefits of ACE inhibition are not homogeneous and are largely confined to high-risk patients who have subjective or objective evidence of left ventricular (LV) dysfunction. How long treatment should continue is a vexed question, which also arises with other agents, for example beta-blocker use after MI. The AIREX study assessed the long-term magnitude and duration of the survival benefits observed with ramipril in patients after MI who have clinically defined heart failure. The mortality status of all 603 patients recruited from the UK centres involved in the AIRE study was verified at an extended 5-year follow-up (3 years after the AIRE study closed). Ramipril assignation was associated with a 36% relative and a 11% absolute mortality risk reduction. These findings strongly support the view to select patients on the basis of impaired LV function and reinforce the previously reported conclusions of the "selective" ACE inhibition post-MI trials. Using this approach, the survival benefit is not only of large magnitude but also sustained over many years. These results also argue for life-long treatment with an ACE inhibitor, once a decision to treat an individual patient after MI has been made.