Bypass grafting operations using conventional technique with off-pump coronary artery bypass grafting in two identical groups conducted at the Penang Hospital (1999-2000)

This is a prospective study conducted at the Department of Cardiothoracic Surgery, Penang Hospital, Penang, with a total of one hundred patients were studied over a period of one year between January 1999 to January 2000. Fifty patients who had undergone coronary artery bypass surgery off-pump (OPCAB) were compared with fifty patients who had undergone coronary artery bypass surgery on the heart-lung machine (CPB). Patients who had associated problems of renal failure, stroke, bronchial asthma and recent myocardial infarction were included in the off-pump CABG surgery. The symptoms did not differ in both the groups. They had experienced angina, decreased effort tolerance, palpitations, with NYHA class IT, ill and IV. The predisposing factors of diabetes mellitus, hypertension, hyperlipidemia, smoking, previous family history of heart disease were studied in both these groups. The same pre-operative investigations were performed in both groups of patients. Chest x-ray, ECG, echocardiography, femoral angiogram were done for these one hundred patients. The intra-and post operative bleeding, pre and post operative renal status, echocardiogram, ECG and chest X-rays were compared. The cost effectiveness of both the OPCAB and CPB procedures were reviewed. There was, generally, a better outcome in patients who had undergone a coronary bypass by the offpump (OPCAB) method as when compared to those by the CPB method. This indicates that more cases can be done by the OPCAB method in the future

Angiopoietin-2 und Fibroblast Growth Factor 23: Prognostische Bedeutung neuer Biomarker im kardiogenen Schock. Eine Substudie der IABP-SHOCK II Studie

Im Rahmen der vorliegenden Dissertation wurde die prognostische Relevanz von Angiopoietin-2 (Ang-2) und Fibroblast Growth Factor 23 (FGF-23) als Prädiktor der 30-Tages sowie Ein-Jahres Mortalität bei Patienten im infarktbedingten kardiogenen Schock (CS) untersucht und dargestellt. Das betrachtete Patientenkollektiv dieser Substudie rekrutierte sich dabei aus den 218, im Rahmen der IABP- SHOCK II Studie in Leipzig eingeschlossenen Patienten. Nach Hospitalisierung und Randomisierung in den jeweiligen Therapiearm (IABP, Nicht-IABP) erfolgte eine prospektiv geplante Blutentnahme an den Tagen eins bis drei. Zur laborchemischen Bestimmung der Serum-, beziehungsweise Plasma Proteinkonzentration mittels ELISA von Ang-2 standen 189, für das Phosphathormon FGF-23 182 Blutproben zur Verfügung. Die 30-Tages Mortalität der untersuchten Substudien-Kohorte betrug 40%, die Ein-Jahres Mortalität 57%. Die vorliegende Arbeit bestätigt Ang-2 als einen starken und unabhängigen negativen Prädiktor des Kurz- und Langzeitverlaufs bei Patienten im CS auf Grund eines akuten Myokardinfarks. Weiterhin zeigt die Auswertung, dass die prognostische Relevanz des betrachteten Biomarkers im zeitlichen Verlauf signifikant zunimmt und verschiedene klinische Parameter wie beispielsweise eine akut eingeschränkte Nierenfunktion oder Blutungskomplikationen unabhängig mit erhöhten Ang-2 Konzentrationen assoziiert sind. Somit sind im infarktbedingten CS hohe Werte von Ang-2 unabhängig mit einem schlechteren klinischen Verlauf des Patienten, sowie dem Reperfusionserfolg und weiteren Komplikationen assoziiert. Patienten der Substudien-Kohorte im infarktbedingten CS waren durch signifikant erhöhte Konzentrationen von FGF-23 charakterisiert. Weiterhin zeigte sich, dass diese signifikant erhöhten Werte unabhängig mit einer deutlich schlechteren Prognose der 30-Tages und Ein-Jahres Mortalität verbunden sind. Diese Assoziation konnte jedoch ausschließlich bei Patienten mit eingeschränkter Nierenfunktion nachgewiesen werden

Effekt eines physiologischen Stressmodells auf den Calcium-Phosphat-Haushalt und den Fibroblast Growth Factor 23 bei nierengesunden Probanden

Ein hoher Plasmaspiegel des phosphaturischen Hormons Fibroblast Growth Factor 23 (FGF-23) ist bei nierenkranken und nierengesunden Menschen in Querschnittsanalysen mit linksventrikulärer systolischer Insuffizienz und in Längsschnittstudien mit kardialen Dekompensationen assoziiert. Unklar ist bislang die Kausalität zwischen einer FGF-23 Erhöhung und kardialer Morbidität. Tierexperimentelle Daten weisen auf eine erhöhte Expression von FGF-23 bei erhöhter Sympathikusaktivität hin und implizieren damit, dass eine chronische Herzinsuffizienz mit konsekutiver Sympathikusaktivierung Ursache und nicht Folge erhöhter FGF-23-Plasmaspiegel sein könnte. Da die klinische Bedeutung dieser tierexperimentellen Verknüpfung noch ungeklärt ist, wurde der Einfluss einer Sympathikusaktivierung im physiologischen Stressmodell einer akuten körperlichen Aktivität auf den Calcium-Phosphat-Haushalt mit Fokus auf FGF-23 untersucht. In die Fit@HOMe Studie wurden 15 männliche Probanden ohne kardiovaskuläre Erkrankungen im Zeitraum von März bis November 2015 eingeschlossen. Bei der Eingangsuntersuchung (Anamnese, körperliche Untersuchung, Echokardiographie, Ruhe- und Belastungs-Elektrokardiogramm) erfolgte eine standardisierte Fahrradergometrie (FE) zur Ermittlung der individuellen anaeroben Schwelle (IAS) nach Stegmann durch eine Laktatbestimmung aus dem Kapillarblut des hyperämisierten Ohrläppchens und der Zielherzfrequenzen. In randomisierter Reihenfolge absolvierten die Probanden im Abstand von einer Woche eine intensive FE bei 90% der IAS (mittlere Belastungsdauer: 60 min) und eine hochintensive FE bei 110% der IAS (mittlere Belastungsdauer: 38 ± 18 min). Messungen von C-terminalem und intaktem FGF-23 und von weiteren Parametern des Calcium-Phosphat-Haushalts erfolgten an vier verschiedenen Zeitpunkten (vor der FE und 5 min, 90 min und 24 h danach). Die Probanden waren im Durchschnitt 25 ± 3 Jahre alt, 1,79 ± 0,07 m groß, 79 ± 13 kg schwer und hatten eine geschätzte mittlere glomeruläre Filtrationsrate von 110 ± 17 ml/min/1,73 m². Da zwei Probanden nicht die Vorgabe der intensiven FE (Belastungszeitraum: 60 min) erreichten, wurden sie bei den nachfolgenden Analysen dieser Belastung nicht berücksichtigt. Weder die intensive noch die hochintensive FE induzierten einen signifikanten Anstieg von C-terminalem FGF-23 (intensive Belastung: prä Median 79,6 [Interquartilsabstand (IQR) 64,9 – 92,4] relative Einheiten (RU)/ml; 5 min post Median 79,0 [IQR 62,3 – 103,2] RU/ml; 90 min post Median 74,9 [IQR 64,2 – 90,1] RU/ml; 24 h post Median 75,2 [IQR 57,5 – 95,3] RU/ml; p = 0,656; hochintensive Belastung: prä Median 71,2 [IQR 48,6 – 94,4] RU/ml; 5 min post Median 71,2 [IQR 55,8 – 97,2] RU/ml; 90 min post Median 75,9 [IQR 63,0 – 134,6] RU/ml; 24 h post Median 64,6 [IQR 46,0 – 84,3] RU/ml; p = 0,184). Auch das intakte FGF-23 zeigte keine Zunahme bei der intensiven (prä Median 39,7 [IQR 34,1 – 50,9] pg/ml; 5 min post Median 40,5 [IQR 35,6 – 47,6] pg/ml; 90 min post Median 42,1 [IQR 30,8 – 49,7] pg/ml; 24 h post Median 43,7 [IQR 39,3 – 55,4] pg/ml; p = 0,635) und bei der hochintensiven (prä Median 34,5 [IQR 29,0 – 42,1] pg/ml; 5 min post Median 41,3 [IQR 31,0 – 48,8] pg/ml; 90 min post Median 39,3 [IQR 33,0 – 50,1] pg/ml; 24 h post Median 39,3 [IQR 32,2 – 56,4] pg/ml; p = 0,135) Belastung. Jedoch stieg die Phosphat-Plasmakonzentration trotz Erhöhung der fraktionellen Phosphatausscheidung, die in der intensiven, nicht jedoch in der hochintensiven FE Signifikanzniveau erreichte. Der Calcium-Plasmaspiegel stieg bei hochintensiver, nicht jedoch bei intensiver Belastung mit Abnahme der fraktionellen Calciumausscheidung. Die Daten unserer Studie untermauern die, in bisherigen Studien postulierte, Hypothese nicht, dass eine Sympathikusaktivierung einen signifikanten FGF-23 Anstieg induziert. Welche anderen Faktoren FGF-23 physiologisch und pathophysiologisch regulieren, sollte in weiteren Arbeiten untersucht werden. Nachfolgend wäre zu prüfen, ob diese Faktoren durch therapeutische Interventionen zur Senkung von FGF-23 führen könnten. In einem letzten Schritt sollte geprüft werden, ob eine solche Senkung von FGF-23 in randomisierten klinischen Studien den erhofften kardiovaskulären Vorteil erbringt.Both in patients suffering from chronic kidney disease and individuals with intact kidney function, high plasma fibroblast growth factor 23 (FGF-23) levels are cross-sectional related to left ventricular systolic dysfunction. Moreover, they predict future cardiac decompensations in chronic kidney disease patients and among individuals with normal renal function. The pathophysiologic pathways by which elevated plasma FGF-23 may induce cardiovascular morbidity are largely unknown. In animal studies, high sympathetic activity induces FGF-23 expression, which suggests that chronic heart failure with consecutively increased sympathetic activity may induce, rather than follow, high FGF-23 plasma levels. As the clinical relevance of these findings has been unknown so far, we aimed to investigate the influence of sympathetic activity on calcium phosphate regulation, focussing on FGF-23, in a physiological stress model of physical activity. Between March and November 2015, 15 male participants without cardiovascular disease were recruited into the Fit@HOMe study. All participants underwent physical examination, echocardiography, electrocardiogram at rest, and an exercise electrocardiogram; additionally, a standardized questionnaire was completed by all participants. A standardized bicycle ergometry was performed in order to define the individual anaerobic threshold (IAT; according to the protocol suggested by Stegmann via capillary blood analyses) and to determine the target heart rate. In randomized order, all participants absolved an intensive bicycle ergometry with 90% of the IAT (average load time of 60 min) and highly-intensive bicycle ergometry with 110% of the IAT (average load time of 38 ± 18 min), with an interval of seven days between the first and the second test. At four time points (before the ergometry and after 5 min, 90 min and 24 h) C-terminal, intact FGF-23 and further calcium phosphate metabolism parameters were measured. The participants were 25 ± 3 years of age, had a mean height and weight of 1.79 ± 0.07 m and 79 ± 13 kg, respectively, and a mean eGFR of 110 ± 17 ml/min/1.73 m². Two participants did not tolerate the workload of the intensive bicycle ergometry for 60 minutes; thus they were excluded from the corresponding analyses. Neither the intensive, nor the highly-intensive bicycle ergometry induced a significant rise of C-terminal (intensive load: pre median 79.6 [interquartile range (IQR) 64.9 – 92.4] relative units (RU)/ml; 5 min post median 79.0 [IQR 62.3 – 103.2] RU/ml; 90 min post median 74.9 [IQR 64.2 – 90.1] RU/ml; 24 h post median 75.2 [IQR 57.5 – 95.3] RU/ml; p = 0.656; highly intensive load: pre median 71.2 [IQR 48.6 – 94.4] RU/ml; 5 min post median 71.2 [IQR 55.8 – 97.2] RU/ml; 90 min post median 75.9 [IQR 63.0 – 134.6] RU/ml; 24 h post median 64.6 [IQR 46.0 – 84.3] RU/ml; p = 0.184). Intact FGF-23 did also not increase with either intensive (pre median 39.7 [IQR 34.1 – 50.9] pg/ml; 5 min post median 40.5 [IQR 35.6 – 47.6] pg/ml; 90 min post median 42.1 [IQR 30.8 – 49.7] pg/ml; 24 h post median 43.7 [IQR 39.3 – 55.4] pg/ml; p = 0.635) or highly-intensive (pre median 34.5 [IQR 29.0 – 42.1] pg/ml; 5 min post median 41.3 [IQR 31.0 – 48.8] pg/ml; 90 min post median 39.3 [IQR 33.0 – 50.1] pg/ml; 24 h post median 39.3 [IQR 32.2 – 56.4] pg/ml; p = 0.135) workload. However, with intensive (but admittedly not with highly-intensive) workload plasma phosphate increased despite rising urinary fractional phosphate excretion. Plasma calcium rose and fractional calcium excretion decreased during highly-intensive, but not during the intensive load. The results of our study are not in line with experimental data which suggested that increased sympathetic activity raise plasma FGF-23 levels. As a next step, alternative physiologic and pathophysiologic regulators of FGF-23 should be identified. Subsequently, it has to be studied in how far therapeutic interventions that target these regulatory factors will decrease plasma FGF-23. In a final step, it has to be analyzed in how far such interventions that lower plasma FGF-23 will also exert beneficial cardiovascular effects

Acute kidney injury after ascending aorta and aortic arch replacement surgery with moderate hypothermia, circulatory arrest and cardiopulmonary bypass

The correlation between deep hypothermic circulatory arrest (DHCA) and cardiopulmonary bypass (CPB) and their effect on renal function is still not clear enough. Renal failure after surgical replacement of ascending aorta in DHCA und CPB in patients due to aneurysm or calcification represents nowadays a major concern. This major study focused on the impact of DHCA and CPB on renal function in those patients. In the presented retrospective cohort study, the database for Kiel University clinic was searched for patients with aortic arch and aortic ascending replacement surgeries with HCA and CPB techniques. Between January 1, 2001, and December 31, 2017. 1359 patients were found in our database with different causes for those operations such as ascending aortic and aortic arch -aneurysm, -dissections or -calcifications, who were operated upon. The patient records were abstracted, and the data were entered into a database and then revised for accuracy by randomly checking chart data with data on the computer. Pre- and postoperative renal function are observed and documented. Acute kidney injury (AKI) was classified according to the current ‘Kidney Disease: Improving Global Outcomes’ (KDIGO} Guidelines. The potential correlation of the length of DHCA-CPBT and worsening renal function was evaluated using Spearman’s rank correlation. The data obtained from our analysis outlined the predictive role of longer moderate HCA and CPB times a for AKI. The complex multifactorial pathophysiology plays an underlying prognostic role regarding the outcome for this life-threatening complication and requires more focused clinical trials to illustrate the contradicting results from the previous analyses regarding the causing pathophysiology. In addition to that we found out that the incidence of AKI after ascending aorta and aortic arch replacement surgery using moderate HCA and CPB is approximately 15 %. And those patients with Postopertaitve AKI have an increase in the mortaliy rate by more than 6 times and 3 times longer ICU sta

Association of Gamma Glutamyl Transferase with Acute Coronary Syndrome and correlation with in-hospital outcomes

BACKGROUND : Although traditionally associated with alcoholic liver disease, recent studies have shown evidence of correlation between elevated Gamma-glutamyltransferase (GGT) and atherosclerotic heart disease. This is said to be due to its role in the generation of reactive oxygen species in the presence of iron. It is independently correlated with conditions associated with increased atherosclerosis, such as obesity, elevated serum cholesterol, high blood pressure and myocardial infarction. It is also demonstrated that serum GGT activity is an independent risk factor for myocardial infarction and cardiac death in patients with coronary artery disease. AIM : 1. To study the correlation between rise in GGT levels and different subsets of Acute Coronary Syndrome. 2. To study the correlation between GGT and risk of Major Adverse Cardiovascular Events(MACE). MATERIALS AND METHODS : This is a cross sectional study conducted at Government Royapettah Hospital and patients admitted with Acute Coronary Syndrome in our ICU were selected. GGT levels were measured for all patients in a standardized manner and cases were observed for five days in the hospital for adverse events. This study was done for a time period between May 2013 to October 2013 and 75 patients with ACS were included. RESULTS AND OBSERVATIONS : Serum GGT levels were significantly elevated in both the STEMI and NSTEMI subsets but not in the unstable angina subset. The mean GGT value for patients who suffered complications is 90.22. The mean value for patients without MACE is a significantly less 46.44. There was also found to be correlation between GGT and presence of hypertension, LV dysfunction, total cholesterol and LDL levels. CONCLUSION : Gamma glutamyltransferase levels were significantly elevated above normal in patients presenting with acute coronary syndrome. GGT levels were independently correlated with STEMI and NSTEMI but had no correlation with unstable angina. There was a significant correlation between GGT levels and incidence of left ventricular systolic LV dysfunction. The mean value of GGT was significantly elevated in patients who suffered from major adverse cardiovascular events. Patients with significantly elevated GGT values may, in future, be referred for early invasive revascularization procedures like PCI/CABG. In conclusion, as concerns ischemic heart disease, GGT assay seems to have the features of a good prognostic marker with optimal sensitivity of the diagnostic assay and it helps improve our ability to predict adverse events in CAD. Further its prognostic impact can be utilized in risk stratification and the need for urgent therapeutic intervention

Proceedings of the Department of Cardiology at the University of Tartu

http://www.ester.ee/record=b1275218*es

Comparison of estimations versus measured resting oxygen consumption in patients with heart failure and reduced ejection fraction undergoing right heart catheterization

Affecting close to 6 million people in the United States, heart failure (HF) represents the final stage of several diseases of the heart and is commonly defined as a reduction in the heart's ability to circulate blood. Cardiac output during right heart catheterization is an important variable used in patient selection for advanced therapies, such as cardiac transplantation and left ventricular assist device implantation. It is common practice to utilize the Fick method to determine the cardiac output (cardiac output = oxygen consumption [VO2]/arteriovenous oxygen difference) inputting estimated VO2 from one of three published empirical formulae. However, these estimation equations have not been validated in patients with HF. The purpose of this study was to determine the accuracy of three widely used equations for the estimation of VO2 compared to direct breath-by-breath measurement of VO2 and determine to what extent clinically significant error occurs in patients with HF and reduced ejection fraction (HFrEF). Forty-four patients with HFrEF undergoing routine cardiac catheterization (65.9% male, 65.9% Caucasian, 64.5 &plusmn 10.7 years old) performed 10 minutes of ventilatory gas exchange immediately following catheterization procedures, and averaged results of the last five minutes were compared to the derived estimations by: LaFarge & Miettinen, Dehmer et al. and Bergstra et al. (estimated - measured). Single-sample t-tests found the mean difference between the estimation of LaFarge & Miettinen was not significant (-10.3 ml/min &plusmn 6.2 SE, p=0.053), but significant differences were found with Dehmer et al. (16.0 ml/min &plusmn 6.4 SE, p=0.008) and Bergstra et al. (40.6 ml/min &plusmn 6.4 SE, p2 and underestimation in patients with higher VO2 for all equations. Bland-Altman plots and single-sample t-tests of dichotomous groups (sex, pulmonary hypertension and aldosterone antagonist medication) did not identify a subgroup where any of the equations were acceptable. The rate of &ge25% error in the estimates of the LaFarge & Miettinen, Dehmer et al. and Bergstra et al. equations occurred in 11%, 23% and 45% (respectively) of the patients. Clinically significant error (misclassification) in the cardiac index derived from the Lafarge & Miettinen, Dehmer et al. and Bergstra et al. equations for three clinically important classifications: cardiogenic shock - 20.5%, 22.7% and 31.8%; hypoperfusion - 15.9%, 15.9% and 25%; abnormal - 13.6%, 13.6% and 15.9%, respectively. Exploring possible HFrEF-specific equations, linear regression modeling was performed with 34 patients. Two models were developed: (Model 1) VO2=-10.76+(127.74*body surface area)+(aldosterone antagonist [prescribed=1, not prescribed=-1]*22.15); (Model 2) VO2=149.4+(sex [male=1, female=-1]*25.41)+(aldosterone antagonist [prescribed=1, not prescribed=-1]*28.34). Bland-Altman plots and t-tests with the remaining 10 patients yielded limits of agreement outside of acceptable limits despite lack of significant differences between the estimated and measured VO2 for Model 1 and Model 2 (11.0 ml/min &plusmn 10.7 SE, p=0.165; 12.4 ml/min &plusmn 0.249, p=0.249). These findings do not support the use of these empirical formulae to estimate the resting VO2 in patients with HFrEF undergoing right heart catheterization. The direct measurement of the resting VO2 should be the primary method applied to the Fick equation for cardiac output