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system resulted in ischemia. Myocardial ischemia is one of the typical cardiac conditions that produce impaired myocardial relaxation. Thus, these alterations in the left ventricular systolic and diastolic functions, which generally occur during ischemia, were observed [7]. We observed that LV ejection fraction decreased in the majority of our patients (Fig. 1). We think that caffeine induced ischemia, which in turn caused a decrease in ejection fraction, in these patients with advanced CAD and hypertension. However, patients with end stage coronary disease with no residual cardiac reserve had LV ejection fraction unchanged. In addition, some of the non-responding patients might have insensitive receptors to caffeine. Conversely, the patients whose LV ejection fraction increased apparently still had the preserved cardiac reserve to respond to caffeine's stimulatory effect on the adrenergic nervous system, thus LV ejection fraction increased in these patients. A recent study showed that caffeine had no acute effect on RV function in healthy subjects [8]. We also found that caffeine did not affect the right ventricular systolic or diastolic function in patients with CAD. To our knowledge, this is the first report of the effects of caffeine on RV functions in patients with CAD. In conclusion, the present study demonstrates that caffeine can raise blood pressure, impair left ventricular systolic and diastolic functions in patients with CAD. Therefore, caution is advised if, patients inadvertently consume moderate or high amounts of coffee before resting or stress
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echocardiographic examination. Right ventricular function does not change significantly with caffeine. The authors gratefully acknowledge Dr. Guzin Fidan Yaylali for her helpful contributions to the figures.
References [1] Connolly HM, Oh JK. Echocardiography. In: Bonow Mann, Zipes Libby, editors. Braunwald's heart disease. Philadelphia: Elsevier; 2012. p. 224. [2] Hartley TR, Sung BH, Pincomb GA, Whitsett TL, Wilson MF, Lovallo WR. Hypertension risk status and effect of caffeine on blood pressure. Hypertension 2000;36:137–41. [3] Hartley TR, Lovallo WR, Whitsett TL. Cardiovascular effects of caffeine in men and women. Am J Cardiol 2004;93:1022–6. [4] Papaioannou TG, Karatzi K, Karatzis E, Papamichael C, Lekakis JP. Acute effects of caffeine on arterial stiffness, wave reflections, and central aortic pressures. Am J Hypertens 2005;18:129–36. [5] Karatzis E, Papaioannou TG, Aznaouridis K, et al. Acute effects of caffeine on blood pressure and wave reflections in healthy subjects: should we consider monitoring central blood pressure? Int J Cardiol 2005;98:425–30. [6] Yu CM, Sanderson JE, Marwick TH, Oh JK. Tissue Doppler imaging a new prognosticator for cardiovascular diseases. J Am Coll Cardiol 2007;49:1903–14. [7] Connolly HM, Oh JK. Echocardiography. In: Bonow Mann, Zipes Libby, editors. Braunwald's heart disease. Philadelphia: Elsevier; 2012. p. 222. [8] Giacomin E, Palmerini E, Ballo P, Zacà V, Bova G, Mondillo S. Acute effects of caffeine and cigarette smoking on ventricular long-axis function in healthy subjects. Cardiovasc Ultrasound 2008;6:9.
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Contemporary clinical spectrum of constrictive pericarditis: A 10-year experience☆ Lilia Oreto a, Alexander Mayer b, Maria Chiara Todaro a, Naoyo Mori c, David C. Kress d, Leonard H. Kleinman d, Suhail Allaqaband b, Tanvir Bajwa b, Timothy E. Paterick b, A. Jamil Tajik b, Bijoy K. Khandheria b,⁎ a
Clinical and Experimental Department of Medicine and Pharmacology, University of Messina, Messina, Italy Aurora Cardiovascular Services, Aurora Sinai/Aurora St. Luke's Medical Centers, University of Wisconsin School of Medicine and Public Health, Milwaukee, WI, USA Center for Urban Population Health, University of Wisconsin-Milwaukee, Milwaukee, WI, USA d Aurora Medical Group, Cardiovascular and Thoracic Surgery, Aurora St. Luke's Medical Center, Milwaukee, WI, USA b c
a r t i c l e
i n f o
Article history: Received 14 June 2012 Accepted 24 June 2012 Available online 18 July 2012 Keywords: Constrictive pericarditis Pericardiectomy Outcomes Left ventricular dysfunction
To the Editor: Constrictive pericarditis (CP) is characterized by the presence of a rigid and often thickened pericardium encasing the ventricles, which leads to impaired ventricular diastolic filling. Differentiating CP from other causes of impaired diastolic function is challenging [1,2].
☆ Grant support: None. ⁎ Corresponding author at: Aurora Cardiovascular Services, 2801 W. Kinnickinnic River Parkway, #845, Milwaukee, WI 53215, USA. Tel.: +1 414 649 3909; fax: + 1 414 649 3529. E-mail address:
[email protected] (B.K. Khandheria).
However, surgical treatment with pericardiectomy results in dramatic improvement of heart failure symptoms [1,3]. Therefore, the earlier a pericardiectomy is performed, the better the long-term outcome and symptom-free survival [1,3]. We studied the clinical spectrum and outcomes of CP in a tertiary care hospital. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology. We retrospectively reviewed clinical characteristics and diagnostic imaging of 43 patients with surgically proven CP who were admitted to Aurora St. Luke's Medical Center from January 2000 to December 2009. Either partial or complete pericardiectomy was performed in all patients. Perioperative mortality was defined as death from any cause occurring within 30 days postsurgery. Median follow-up was 10 months (interquartile range, 1.5–59.3 months). Continuous variables are summarized as medians with interquartile range. Discrete variables are described as counts with percentages. Univariate binary logistic regression analysis was performed to calculate odds ratio (OR) with 95% confidence interval (CI) and to examine the predictive effect of each factor on the risk of endpoint (perioperative mortality and overall mortality). All statistical analyses were performed using SAS Version 9.2 (SAS Institute Inc., Cary, North Carolina) and p values b0.05 were considered statistically significant (two-tailed). During the 10-year period, CP was surgically proven in 43 patients, aged 54 to 73 years (median 67 years; mean age 63.6); 33 patients (77%) were male. Etiology and clinical characteristics are
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Table 1 Patient characteristics. Characteristic Demographics Median age, years, (IQR) Gender Male Female Baseline characteristics Diabetes mellitus Hypertension Hypercholesterolemia Coronary artery disease Ejection fraction b40% Chronic kidney disease Cerebrovascular accident Atrial fibrillation Anemia Cirrhosis Chronic obstructive pulmonary disease Smoking Alcohol Median BNP (IQR) Type of surgery Pericardial Pericardial + other cardiac surgeries On-pump Median follow-up, months (IQR) Dyspnea Peripheral edema Anasarca/ascites Atrial fibrillation (at presentation) Chest pain Pleural effusion Diagnostic tools used Chest X-ray Cardiac catheterization CT/CMR Echocardiography Electrocardiography Degree of surgery Complete Partial
Overall (n = 43) 67 (54–73) 33 (76.7%) 10 (23.3%) 14 (32.6%) 23 (53.5%) 17 (39.5%) 12 (27.9%) 9 (20.9%) 14 (32.6%) 1 (2.3%) 13 (30.2%) 3 (7.0%) 2 (4.7%) 4 (9.3%) 28 (65.1%) 6 (14.0%) 343 (114–782) 28 (65.1%) 15 (34.9%) 20 (46.5%) 9.6 (1.5–59.3) 39 (90.7%) 31 (72.1%) 14 (32.6%) 2 (4.7%) 9 (20.9%) 9 (20.9%) 5 (17%) 25 (81%) 20 (46%) 5 (16%) 9 (28%) 43 (100%) 31 (72.1%) 12 (27.9%)
Data presented as no. (%) unless otherwise indicated. BNP: B-type natriuretic peptide; CT: computed tomography; CMR: cardiac magnetic resonance imaging; IQR: interquartile range.
summarized in Table 1. Different diagnostic techniques contributed variably to the diagnosis (Table 1). All patients underwent pericardiectomy, and it was combined with other cardiac surgeries in 35% of cases. Overall long-term all-cause mortality was 39%. Perioperative (30day) mortality was 16%, while 10-month median survival was 67%. A significant association with systolic dysfunction was noted. Ejection fraction (EF) b40% predicted perioperative mortality (OR: 8.27, 95% CI: 1.41–48.54; p=0.019). However, prior cardiac surgery was a predictor of reduced long-term survival (OR: 6.82, 95% CI: 1.47–31.61; p = 0.014) (Table 2). CP is a heterogeneous disease and diagnosis still remains difficult in contemporary clinical practice [4,5]. The more common etiologies for CP in our study were idiopathic, previous open heart surgery, previous pericarditis and radiation to the chest (Fig. 1). Our rates for each cause are similar to those reported by other recent studies [2]. In contrast, the etiologic spectrum of CP is widely different today than it was prior to 1980: idiopathic and infectious CP were much more frequently reported than postsurgical or postradiation CP [4]. Clinical characteristics at presentation in this study were similar to those reported by Ling et al. [4], particularly peripheral edema, pleural effusion and atrial fibrillation. Compared with previous studies [4,6], our perioperative mortality (16%) is higher, and the only significant predictive factor is left ventricular dysfunction (p = 0.019), represented by low EF (b40%). Perioperative mortality after pericardiectomy is reported in the literature over the last 20 years to range from 3.4% to 10.5% [4,6]. However, a comparison with other studies is not feasible, since most do not report EF or only report nearly normal EF. Instead of EF, most studies report New York Heart Association (NYHA) functional class, a somewhat subjective evaluation. Nevertheless, perioperative mortality in those studies is usually statistically higher in patients with NYHA class III or IV. Moderately or severely reduced EF is a widely known risk factor that strongly influences perioperative and postoperative mortality [7,8]. Therefore, the high prevalence of systolic dysfunction in our population is the major predictor of higher perioperative mortality. We can hypothesize that the high prevalence of left ventricular systolic dysfunction in our population is likely related to a long-lasting untreated pericardial constriction.
Table 2 Univariate logistic regression analysis. Variable Demographics Age Gender Baseline characteristics Low QRS voltage Diabetes mellitus Hypertension High cholesterol Coronary artery disease Ejection fraction b 40% Chronic kidney disease Atrial fibrillation Smoking Alcohol Brain natriuretic peptide Type of surgery Pericardiectomy vs. pericardiectomy + other cardiac surgeries On-pump Etiology Idiopathic Cardiac surgery CI: confidence interval; OR: odds ratio. a No women died within 30 days.
Perioperative mortality (n = 7)
Overall mortality (n = 17)
OR (95% CI)
p value
1.01 (0.94–1.08) NAa
0.807
1.02 (0.97–1.07) 1.03 (0.24–4.35)
0.445 0.973
0.83 1.71 0.60 1.18 1.04 8.27 0.80 0.91 1.41 1.03 1.00
0.882 0.528 0.540 0.844 0.966 0.019 0.806 0.909 0.703 0.978 0.489
1.83 (0.37–8.94) 1.23 (0.34–4.49) 1.43 (0.42–4.91) 1.12 (0.32–3.90) 2.94 (0.75–11.60) 2.29 (0.52–10.18) 0.79 (0.21–2.95) 0.34 (0.08–1.50) 0.97 (0.27–3.50) 0.73 (0.12–4.53) 1.001 (0.999–1.004)
0.456 0.757 0.571 0.859 0.124 0.276 0.722 0.155 0.964 0.738 0.209
(0.08–9.25) (0.33–8.93) (0.12–3.08) (0.23–6.08) (0.17–6.26) (1.41–48.54) (0.14–4.75) (0.15–5.43) (0.24–8.34) (0.10–10.50) (0.99–1.01)
OR (95% CI)
p value
1.41 (0.24–8.34) 0.84 (0.16–4.29)
0.703 0.832
2.38 (0.61–9.33) 0.70 (0.20–2.41)
0.212 0.7
1.33 (0.26–6.87) 1.20 (0.20–7.30)
0.736 0.843
0.57 (0.16–2.09) 6.82 (1.47–31.61)
0.395 0.014
Letters to the Editor
Fig. 1. Etiologic spectrum of surgically proven constrictive pericarditis in our patient population.*Miscellaneous includes autoimmune disease (rheumatoid arthritis), pacemaker implantation complicated by subacute tamponade and carcinoid and metastatic cancer.
Two important points need consideration: first, CP is a relatively rare disease and its clinical manifestations are often insidious, which makes diagnosis challenging. This happens especially if comorbidities are present, which may explain the clinical signs and symptoms of heart failure, leading to a delay in diagnosis. Second, prolonged constriction itself is thought to result in myocardial atrophy. Different pathologic studies have attributed myocardial atrophy in CP to disuse of myocardial fibers, but mainly in regard to myocardial ischemia, which occurs as a result of myocardial compression from external rigid pericardium as well as from internal elevated intraventricular pressures [9]. A strong association between etiology and mortality has been reported by Bertog et al. [6]. In our population long-term mortality was significantly higher in patients with previous open heart surgery (p = 0.014): 70% of all long-term deaths were patients who underwent prior coronary artery bypass, valve replacement or heart transplant surgery. We suspect that the reason for worse outcome in this subgroup of patients may be concomitant myocardial dysfunction, which is common in patients with a history of coronary artery disease, valvular disease or end-stage heart failure. However, long-term mortality is better in patients with idiopathic CP because the disease process, most of the time, is limited to the pericardium, although long-standing untreated CP may involve the myocardium and result in worse prognosis.
0167-5273/$ – see front matter © 2012 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2012.06.083
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Given the low prevalence and the complexity in diagnosis of CP, it may be advisable to adopt a higher level of suspicion in high-risk patients, especially those with previous cardiac surgery or chest radiation, to avoid delay in diagnosis. Pericardiectomy is the treatment of choice for CP and it should be performed as soon as possible to relieve pericardial restraint. Unfortunately, we may not see such a dramatic result when the myocardium also is affected, as it occurs in patients with long-standing undiagnosed CP, as well as in patients with prior chest radiation or history of open heart surgery [1,3]. For this reason, prompt intervention is recommended as there is evidence that if pericardiectomy is performed before the advent of systolic dysfunction, it can lead to a favorable outcome [3]. The authors gratefully acknowledge Barbara Danek, Joe Grundle and Katie Klein for their editorial preparation of the manuscript and Brian Miller and Brian Schurrer for their help with the figure.
References [1] Sengupta PP, Eleid MF, Khandheria BK. Constrictive pericarditis. Circ J 2008;72:1555–62. [2] Schwefer M, Aschenbach R, Heidemann J, Mey C, Lapp H. Constrictive pericarditis, still a diagnostic challenge: comprehensive review of clinical management. Eur J Cardiothorac Surg 2009;36:502–10. [3] Chowdhury UK, Subramaniam GK, Kumar AS, et al. Pericardiectomy for constrictive pericarditis: a clinical, echocardiographic, and hemodynamic evaluation of two surgical techniques. Ann Thorac Surg 2006;81:522–9. [4] Ling LH, Oh JK, Schaff HV, et al. Constrictive pericarditis in the modern era: evolving clinical spectrum and impact on outcome after pericardiectomy. Circulation 1999;100:1380–6. [5] Dal-Bianco JP, Sengupta PP, Mookadam F, Chandrasekaran K, Tajik AJ, Khandheria BK. Role of echocardiography in the diagnosis of constrictive pericarditis. J Am Soc Echocardiogr 2009;22:24–33. [6] Bertog SC, Thambidorai SK, Parakh K, et al. Constrictive pericarditis: etiology and cause-specific survival after pericardiectomy. J Am Coll Cardiol 2004;43:1445–52. [7] Nashef SA, Roques F, Hammill BG, et al. Validation of European System for Cardiac Operative Risk Evaluation (EuroSCORE) in North American cardiac surgery. Eur J Cardiothorac Surg 2002;22:101–5. [8] Ha JW, Oh JK, Schaff HV, et al. Impact of left ventricular function on immediate and long-term outcomes after pericardiectomy in constrictive pericarditis. J Thorac Cardiovasc Surg 2008;136:1136–41. [9] Gregory MA, Whitton ID, Cameron EW. Myocardial ischaemia in constrictive pericarditis — a morphometric and electron microscopical study. Br J Exp Pathol 1984;65:365–76.
