Delayed diagnosis of chronic Q fever and cardiac valve surgery.

Untreated chronic Q fever causes a high number of complications and deaths. We present cases of chronic Q fever that were not diagnosed until after the patients underwent cardiac valve surgery. In epidemic areas, Q fever screening of valve surgery patients secures early initiation of treatment and can prevent illness and death.

Prevalence of chronic Q fever in patients with a history of cardiac valve surgery in an area where Coxiella burnetii is epidemic.

Chronic Q fever develops in 1 to 5% of patients infected with Coxiella burnetii. The risk for chronic Q fever endocarditis has been estimated to be ≈ 39% in case of preexisting valvulopathy and is potentially even higher for valvular prostheses. Since 2007, The Netherlands has faced the largest Q fever outbreak ever reported, allowing a more precise risk estimate of chronic Q fever in high-risk groups. Patients with a history of cardiac valve surgery were selected for microbiological screening through a cardiology outpatient clinic in the area where Q fever is epidemic. Blood samples were analyzed for phase I and II IgG against C. burnetii, and if titers were above a defined cutoff level, C. burnetii PCR was performed. Chronic Q fever was considered proven if C. burnetii PCR was positive and probable if the phase I IgG titer was ≥ 1:1,024. Among 568 patients, the seroprevalence of C. burnetii antibodies (IgG titer greater than or equal to 1:32) was 20.4% (n = 116). Proven or probable chronic Q fever was identified among 7.8% of seropositive patients (n = 9). Valve characteristics did not influence the risk for chronic Q fever. Patients with chronic Q fever were significantly older than patients with past Q fever. In conclusion, screening of high-risk groups is a proper instrument for early detection of chronic Q fever cases. The estimated prevalence of chronic Q fever is 7.8% among seropositive patients with a history of cardiac valve surgery, which is substantially higher than that in nonselected populations but lower than that previously reported. Older age seems to increase vulnerability to chronic Q fever in this population.

Chronic Q fever-related dual-pathogen endocarditis: case series of three patients.

Following Coxiella burnetii infection, there is a 1 to 5% risk of chronic Q fever. Endocarditis, mycotic aneurysm, and vascular prosthesis infection are common manifestations. We present three patients with endocarditis by C. burnetii concomitant with another bacterial pathogen. Chronic Q fever should therefore be considered in all endocarditis patients in regions where Q fever is endemic.

Impact of infarct location on left ventricular ejection fraction after correction for enzymatic infarct size in acute myocardial infarction treated with primary coronary intervention.

BACKGROUND: Left ventricular function and infarct size are strong predictors for prognosis after acute myocardial infarction (MI). Anterior MI is associated with greater reduction of left ventricular ejection fraction (LVEF) and worse prognosis. Our objective was to study whether the impact of infarct size on global LVEF is dependent of infarct location. METHODS: We analyzed 888 patients treated with primary percutaneous coronary intervention for acute MI. Enzymatic infarct size and LVEF within 1 week were measured. In 490 patients (55%), LVEF was measured a second time at 6 months. RESULTS: Every 1000 U/L of cumulative lactate dehydrogense release corresponded to a decrease of 4.7% (95% CI 4.1-5.3) in LVEF measured within 1 week post MI for left anterior descending coronary artery (LAD)-related infarcts and to a decrease of 2.4% (95% CI 1.7-3.1) in LVEF measured within 1 week post MI for non-LAD-related infarcts (P < .0001). Left ventricular ejection fraction measured 6 months post MI showed a decrease for every 1000 U/L cumulative lactate dehydrogense release of 4.8% (95% CI 4.2-5.3) for LAD and 2.4% (95% CI 1.7-3.1) for non-LAD-related infarcts (P < .0001). Multivariate correction for relevant clinical and angiographic data did not change these results. CONCLUSION: In patients with a first acute MI treated with primary percutaneous coronary intervention, LAD-related infarcts show for a similar amount of myocardial necrosis as determined by enzymatic infarct size, a lower residual LVEF when compared with non-LAD-related infarcts.

Effect of coronary occlusion site on angiographic and clinical outcome in acute myocardial infarction patients treated with early coronary intervention.

In acute myocardial infarction that is treated with thrombolysis, proximal coronary artery occlusion is associated with worse prognosis, irrespective of the infarcted artery. Primary percutaneous coronary intervention (PCI) is currently the treatment of choice for ST-segment elevation acute myocardial infarction. Therefore, we evaluated the prognostic significance of proximal versus distal coronary artery occlusion in patients with acute myocardial infarction that was treated with primary PCI. Between 1994 and 2001, patients with a first acute myocardial infarction that was treated with primary PCI were analyzed. A lesion was considered proximal if it was located proximal to the first diagonal branch in the left anterior descending coronary artery (LAD), the first marginal obtuse branch in the left circumflex coronary artery, and the first right acute marginal branch in the right coronary artery. Lesions distal of these side branches were considered distal. In total, 1,468 patients were analyzed. Left ventricular ejection fraction (LVEF) for proximal LAD lesions was lower than that for distal ones (37 +/- 11% vs 42 +/- 11%, p <0.0001). Adjusted relative risk of 3-year mortality for proximal versus distal LAD was 4.04 (95% confidence interval 1.95 to 8.38). In patients with infarcts related to the right or left circumflex coronary artery, no significant association between lesion location and LVEF or mortality was seen. No difference was seen in adjusted 3-year mortality between distal LAD and non-LAD-related infarcts (p = 0.145). In conclusion, our analysis shows that, even in patients with acute myocardial infarction that is treated with primary PCI, infarcts related to the proximal LAD have the worst 3-year survival and lowest residual LVEF compared with distal LAD or non-LAD-related infarcts.

The predictive value of cumulative lactate dehydrogenase release within the first 72 h of acute myocardial infarction in patients treated with primary angioplasty.

BACKGROUND: In patients with acute myocardial infarction, estimation of infarct size by cumulative lactate dehydrogenase release at 72 h (LDHQ(72)) is a simple and widely used method. Our objective was to study the value of estimating infarct size, by the cumulative release of LDH over 72, 60, 48 and 36 h in predicting left ventricular ejection fraction (LV(ef)) and cardiac death at 1 year. METHODS: In the Zwolle Infarction Study infarct size estimated as LDHQ was calculated in 1224 patients treated with primary percutaneous coronary intervention for acute myocardial infarction between December 1993 and June 2001. Patients were categorized as having small (LDHQ(72)<800 U/L), medium (LDHQ(72) 800-2500 U/L) or large (LDHQ(72)>2500 U/L) myocardial infarction. RESULTS: LDHQ(72) was closely correlated with LDHQ(60), LDHQ(48) and LDHQ(36) (r = 0.998, 0.993 and 0.987, respectively, P <0.0001). The relations between LDHQ infarct size classification and mean LV(ef) (51% vs 45% vs 35%, P <0.001) or cardiac death at 1 year (0-0.3% vs 0.7-1% vs 6-8%) showed a similar pattern, irrespective of whether LDH was measured up to 36, 48, 60 or 72 h. CONCLUSION: Infarct size classification based on LDHQ(36) is an objective and widely available method for early risk stratification in patients treated with primary angioplasty for acute ST-segment elevation myocardial infarction.