Two rare cases of left and right atrial congenital heart disease: cor triatriatum dexter and sinister.
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Adrenergic beta-Agonists↗
Biomedical subjects
E Giannitsis
Publications and source records attributed to E Giannitsis.
Effect of stress-induced reversible ischemia on serum concentrations of ischemia-modified albumin, natriuretic peptides and placental growth factor.
OBJECTIVE: There is controversy whether new biomarkers are able to identify myocardial ischemia in the absence of myonecrosis. METHOD: We measured NT-pro BNP, NT-pro ANP, ischemia-modified albumin (IMA) and placental growth factor (PlGF) in patients undergoing nuclear stress testing for suspected ischemic heart disease. A thallium scan was used for detection of reversible myocardial ischemia and cardiac troponin T (cTnT) for exclusion of stress-induced myonecrosis. Of 195 patients, 24 with reversible and 62 with no perfusion defect were included in the analysis. Plasma levels were measured before, 18 min and 4 h after stress testing. RESULTS: Of the 86 patients, 52 received an exercise stress and 34 dipyridamol. New myonecrosis indicated by cTnT could be excluded in all patients. Plasma levels of NT-pro BNP and NT-pro ANP before testing were significantly higher in patients who later developed reversible perfusion defects (NT-pro BNP 139.00 (58.25/367.01) pg/mL vs 327.45 (120.50/972.85) pg/mL, p<0.05; NT-pro ANP 732.5 (470.0/1220.0) pg/mL vs 1470.0 (694.0/1910.0) pg/mL, p<0.05). Plasma levels of NT-pro BNP, NT-pro ANP and PIGF did not change significantly after stress testing, IMA levels rose significantly after 4 h in patients with and without reversible perfusion defects. CONCLUSION: The elevation of NTpro BNP and NT-pro ANP at baseline may represent the cumulative effect of repeated bouts of myocardial ischemia. A single brief episode of provoked ischemia does not cause a significant increase of the measured biomarkers beside from IMA after exercise stress test potentially indicating skeletal muscle ischemia.
Aged↗
[Risk stratification in the acute coronary syndrome. Diabetes--a diagnostic dilemma].
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Angina, Unstable↗
[Platelet inhibitors from a cardiological viewpoint: evidence based therapy and new concepts for the acute coronary syndrome without ST-segment elevation].
The pathophysiology of the acute coronary syndrome is related to a vulnerable, inflammatory plaque promoting activation and aggregation of platelets. Therefore, the inhibition of platelet function is a primary goal of the treatment of the acute coronary syndrome. In recent years this field has made substantial progress, which is reflected by frequently updated treatment guidelines. New dose regimens and therapeutic strategies, but also innovative pharmacological principles evolved recently. Some of these novel drugs are currently tested in clinical trials. Increasing experience with the currently used platelet inhibitors also revealed potential shortcomings of these substances, such as drug resistance. This review will give a cardiological perspective of some important clinical aspects and new developments in the field of platelet inhibitors.
Acute Disease↗
[Acute chest pain].
Acute chest pain is the leading cause of hospital admissions worldwide and absorbs extensive financial and hospital resources for diagnosis and management. A missed diagnosis of acute myocardial infarction is still associated with a poor outcome and represents one of the most common reasons for lawsuits in the USA. The present article gives a summary on the features of cardiac and non-cardiac chest pain, provides an overview of diagnostic algorithms, and points out the important differential diagnoses.
Acute Disease↗
[Acute posterior myocardial infarct. A typical diagnostic error].
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Biomarkers↗
Effects of intracoronary low-dose enalaprilat as an adjunct to primary percutaneous transluminal coronary angiography in acute myocardial infarction.
Bradykinin accumulation is a potent cardioprotective mechanism underlying angiotensin-converting enzyme (ACE) inhibition in ischemia and/or reperfusion injury. There is, however, concern about treatment with ACE inhibitors in the very early phase of acute myocardial infarction (AMI) due to adverse systemic hemodynamic effects. We tested the hypothesis that cardiac bradykinin metabolism can be influenced by very low doses of intracoronary ACE inhibitors without harmful systemic effects in patients with AMI. Twenty-two patients with AMI in Killip classes II to III who underwent primary percutaneous transluminal coronary angiography (PTCA) were randomized to intracoronary enalaprilat (50 microg) or saline, given immediately after reopening of the infarct-related artery. Hemodynamics and electrocardiograms were monitored continuously and samples for determination of ACE activity, angiotensin II, bradykinin, kininogen, and cardiac marker proteins were collected from pulmonary arterial and central venous blood. Enalaprilat had no adverse effects on systemic hemodynamics, but rather stabilized arterial pressure and cardiac rhythm during reperfusion. Enalaprilat induced a 70% reduction of ACE activity and a significant increase of bradykinin in pulmonary arterial blood. Angiotensin II was not significantly affected by enalaprilat either in pulmonary arterial or in central venous blood. Myoglobin release was lower and the duration of reperfusion arrhythmias was significantly reduced in the enalaprilat group (p <0.05). Thus, in this pilot study, intracoronary enalaprilat infusion in the infarct-related artery is feasible in the setting of primary angioplasty and is safe and well tolerated. Effective cardiac ACE inhibition can be achieved by low-dose intracoronary enalaprilat, which primarily causes a potentiation of bradykinin.
Angioplasty, Balloon, Coronary↗
Admission troponin T level predicts clinical outcomes, TIMI flow, and myocardial tissue perfusion after primary percutaneous intervention for acute ST-segment elevation myocardial infarction.
BACKGROUND: In ST-segment elevation myocardial infarction, a troponin T >/=0.1 microg/L on admission indicates poorer prognosis despite early reperfusion. To evaluate the underlying reason, we studied the value of cardiac troponin T (cTnT) for prediction of outcomes, epicardial blood flow, and myocardial reperfusion after primary percutaneous intervention. METHODS AND RESULTS: Patients (n=140) admitted within 12 hours after onset of symptoms were stratified by admission cTnT. Epicardial and myocardial reperfusion were graded by the TIMI score and by measurement of relative increases of myoglobin, cTnT, and creatine kinase (CK)-MB 60 minutes after recanalization, respectively. cTnT was positive in 64 patients (45.7%) and was associated with longer median time intervals to admission (5.5 versus 3.5 hours, P<0.001) and higher mortality rates after 30 days (12.5% versus 3.9%, P=0.06) and 9 months (14% versus 3.9%, P=0.005). cTnT independently predicted a 3.2-fold risk for incomplete epicardial reperfusion (P=0.03). In addition, cTnT >/=0.1 microg/L was associated with more severely impaired myocardial perfusion despite normal epicardial flow, as indicated by lower 60-minute ratios of myoglobin (2.6 versus 7.6, P=0.007), cTnT (6.6 versus 29.2, P<0.001), and CK-MB (3.5 versus 21.4, P=0.002) and a tendency for less resolution of ST-segment elevations (54% versus 60%, P=0.08). CONCLUSIONS: cTnT predicts poorer clinical outcomes, lower rates of postprocedural TIMI 3 flow, and more severely compromised myocardial perfusion despite normal epicardial flow. Thus, a cTnT-positive patient may require more aggressive adjunctive therapy when treated by percutaneous coronary intervention. The impact of preexisting or evolving microvascular dysfunction and the effect of therapies that target myocardial perfusion require further prospective evaluation.
Aged↗
[Acute heart infarct--new definition and diagnostic techniques].
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Age Factors↗
Troponin T elevation after successful directional atherectomy.
BACKGROUND: The incidence and correlates of postinterventional cardiac troponin T (cTnT) elevation have not been evaluated in patients with successful directional atherectomy (DCA). METHODS: Total creatine kinase (CK) activity, CK-MB mass concentrations and cTnT levels were measured in 36 patients before, and serially 4, 24, 48 and 72 hours after successful DCA. Patients were followed for death, Q-wave infarction, need for emergency bypass surgery, periprocedural vascular complications (transient in-lab vessel closure, side branch compromise, large dissection), and non-Q-wave infarction on ECG. Patients were followed for clinical outcomes and angiographic restenosis for 6 months. Vascular correlates were studied by coronary angiography and intravascular ultrasound before, immediately after and 4 hours after elective and successful DCA. RESULTS: 25 patients (69.4%) had elevated levels of cTnT, whereas CK-MB mass > or = 6 ng/ml and mild elevations of total CK activity were present in only 36.1 and 5.6%, respectively. Elevated cTnT was related to vascular complications in 44% of cases. Inapparent microembolization of platelets or plaque debris was considered responsible for most of the remaining micronecroses. During 6 month follow-up rates of clinical restenosis (44 vs 9%, p = 0.059) tended to be higher in patients with as compared to patients without cTnT release after DCA. CONCLUSION: Successful DCA is associated with postprocedural elevations of cTnT which relate to minor vascular complications and presumably microembolization of platelets or plaque debris. The superior diagnostic performance of cTnT compared to CK-MB mass may relate to more sensitive identification of microinfarction. Further studies are mandatory to confirm the association between elevation of cTnT and risk of restenosis and TVR.
Atherectomy, Coronary↗
Angiographic correlates of a positive troponin T test in patients with unstable angina.
OBJECTIVE: To study the angiographic correlates of cardiac troponin T (cTnT)-positive and -negative patients with unstable angina pectoris. BACKGROUND: A positive cTnT test identifies a high-risk subgroup of unstable angina pectoris patients. Only the high-risk cTnT-positive patients seem to benefit from a more aggressive antithrombotic treatment regimen. The underlying coronary pathology in cTnT-positive and -negative patients that explains the predictive power of cTnT on prognosis and response to antithrombotic therapy is largely unknown. METHODS: A total of 197 subsequently admitted patients with unstable angina pectoris underwent cTnT testing by a rapid bedside assay and early qualitative and quantitative angiography. Long-term follow-up was 12 months. RESULTS: Patients with cTnT-positive tests revealed more critical stenoses of culprit lesions (p =.041), more severe reductions of thrombolysis in myocardial infarction flow grades (p <.037), a higher prevalence of intracoronary thrombus (p =.079), and a poorer left ventricular function (p =.047). The odds ratio of cTnT was 5.8 (p <.0001) for presence of thrombus, reduced thrombolysis in myocardial infarction flow, and/or critical stenosis (>90%), and was 3.1 (p =.005) for presence of three-vessel disease, left main disease, and/or reduced left ventricular ejection fraction. Coronary bypass grafting was more frequently performed in the cTnT-positive group. However, event-free survival was not different in our cohort characterized by a high rate of percutaneous coronary interventions. CONCLUSIONS: A positive cTnT test in patients with unstable angina pectoris indicates presence of more severe coronary artery disease and poorer left ventricular function. This finding could explain the differences in short- and long-term outcome and treatment responses to antithrombotic regimens.
Aged↗
Cardiac troponin T in ST-segment elevation acute myocardial infarction revisited.
Cardiac troponins not only allow for risk stratification and guidance of therapy in unstable angina and non-Q-wave acute myocardial infarction but also may be useful in the diagnostic workup and monitoring of patients with ST-segment elevation myocardial infarction. In clinical practice, troponins are used for confirmation and monitoring of myocardial infarction, noninvasive prediction of reperfusion success after thrombolytic therapy, and noninvasive estimation of infarct size. Accumulating evidence suggests that the measurement of cardiac troponins on admission may represent a relatively novel application that is useful for early risk stratification and prediction of reperfusion success after thrombolysis or primary percutaneous coronary interventions. Potential mechanisms of the predictive power of cardiac troponins are discussed.
Acute Disease↗
Risk stratification in patients with inferior acute myocardial infarction treated by percutaneous coronary interventions: the role of admission troponin T.
BACKGROUND: Cardiac troponin T (cTnT) elevations on admission indicate a high-risk subgroup of patients with ST-segment elevation acute myocardial infarction (AMI). This finding has been attributed to less effective reperfusion after thrombolytic therapy. The aim of this study was to determine the role of admission cTnT on the efficacy of percutaneous coronary interventions (PCIs) in inferior AMI. METHODS AND RESULTS: One hundred fifty-nine consecutive patients with inferior ST-segment AMI were enrolled and followed up for a mean of 448 days. Patients were stratified by cTnT on admission. A cTnT >/=0.1 microg/L was found in 58% of patients. These patients had longer time intervals from onset of symptoms to therapy (P:<0. 001) and higher 30-day (10.8% versus 1.5%, P:=0.027) and long-term (17.2% versus 4.5%, P:=0.023) cardiac mortalities. Rates of the combined end point of death, nonfatal reinfarction, and need for repeated target vessel revascularization procedures were not different in cTnT groups (log rank, 0.69; P:=0.41). PCI was attempted in 93.3% of cTnT-positive and 98.5% cTnT-negative patients (P:=0.24) but was less frequently successful in patients with cTnT >/=0.1 microg/L (77.9% versus 96.9%, P:<0.001). Coronary stenting reduced 30-day and long-term cardiac mortality, particularly among cTnT-positive patients. In a multivariate analysis, cTnT indicated an approximately 5-fold-higher risk (adjusted OR, 4.6; 95% CI, 0.79 to 27.11; P:=0.089) and was a strong albeit not independent risk predictor. CONCLUSIONS: In inferior AMI, a positive admission cTnT is associated with lower success rates of direct PCI and higher rates of cardiac events over the short and long term. These patients benefit from coronary stenting.
Acute Disease↗
Independent prognostic value of cardiac troponin T in patients with confirmed pulmonary embolism.
BACKGROUND: Cardiac troponin T (cTnT) is a sensitive and specific marker, allowing the detection of even minor myocardial cell injury. In patients with severe pulmonary embolism (PE), myocardial ischemia may lead to progressive right ventricular dysfunction. It was therefore the purpose of this study to test the presence of cTnT and its prognostic implications in patients with confirmed PE. METHODS AND RESULTS: Fifty-six consecutive patients with confirmed PE were enrolled in this prospective study. PE was confirmed by pulmonary angiography, lung scan, or echocardiography and subsidiary analyses. Severity of PE was assessed by a clinical scoring system, and cTnT was measured within 12 hours after admission. cTnT was elevated (>/=0.1 microg/L) in 18 (32%) patients with massive and moderate PE but not in patients with small PE. In-hospital death (odds ratio 29. 6, 95% CI 3.3 to 265.3), prolonged hypotension and cardiogenic shock (odds ratio 11.4, 95% CI 2.1 to 63.4), and need for resuscitation (odds ratio 18.0, 95% CI 2.6 to 124.3) were more prevalent in patients with elevated cTnT. cTnT-positive patients more often needed inotropic support (odds ratio 37.6, 95% CI 5.8 to 245.6) and mechanical ventilation (odds ratio 78.8, 95% CI 9.5 to 653.2). After adjustment, cTnT remained an independent predictor of 30-day mortality (odds ratio 15.2, 95% CI 1.22 to 190.4). CONCLUSIONS: cTnT may improve risk stratification in patients with PE and may aid in the identification of patients in whom a more aggressive therapy may be warranted.
Aged↗
Clinical and angiographic outcome of patients with acute inferior myocardial infarction.
OBJECTIVES: This study sought to determine the procedural success and the in-hospital outcome after primary coronary angioplasty in patients with acute inferior myocardial infarction and right ventricular involvement (RVI). BACKGROUND: RVI represents an easily detectable, highly prevalent subset of acute inferior infarction associated with poor outcome even in the era of thrombolysis. Primary PTCA may offer advantages in patients with inferior infarction involving the right ventricle. METHODS: Primary coronary angioplasty with optimal stenting was performed in 87 of 88 consecutive patients presenting within 24 hours after onset of acute inferior myocardial infarction. On the basis of right precordial ST segment elevations at admission, patients were classified into those without (n=61) and those with RVI (n=27). The patients were followed prospectively for angiographic success at 10 days and for in-hospital clinical outcome. RESULTS: Baseline characteristics including age, severity of coronary artery disease, proportion of stent implantation, and occurrence of cardiogenic shock were comparable. Patients with RVI had larger infarct sizes (lactate dehydrogenase level: 962 vs 580 U/l, P=0.03), developed more often complete atrioventricular block (18.5 vs. 2%, p=0.0038), needed more often parasympatholytics (48.1 vs 18.8%, p<0.001), and had a substantially higher incidence of the Bezold-Jarisch reflex (29.6 vs 6.6%, p<0.01) following reperfusion. Success of recanalization therapy acutely and at 10 days, as well as in hospital mortality were similar in patients with and without RVI (88.5 vs. 85.2%, 79.3 vs. 84.7%, 7.4 vs 9.8%). However, patients with RVI revealed a greater lumen gain acutely after PTCA (2.49 vs. 2.13 mm, p=0.025) and experienced less frequently major cardiac events (14.8 vs. 36.1%, p=0.04) which included reinfarction, re-ischemia, coronary bypass grafting, stent thrombosis, and cardiac death. In addition, procedural success was established more rapidly (fluoroscopy time: 10 vs 15 min., p=0.032) and with less contrast material (242 vs 295 ml, p=0.015) in patients with RVI. This is probably due to the more proximal location (84.6 vs 6.6%, p<0.0001) and the larger reference diameter (3.17 vs. 2.79 mm, p=0.03) of the occluded right coronary artery. CONCLUSIONS: Primary PTCA is an appropriate reperfusion strategy in patients with RVI. Further comparative studies are required to compare the effectiveness of primary PTCA with early thrombolytic therapy in this high risk setting.
Aged↗
Effectiveness of end-tidal carbon dioxide tension for monitoring thrombolytic therapy in acute pulmonary embolism.
OBJECTIVE: In acute massive pulmonary embolism with hemodynamic instability, monitoring of pulmonary artery pressure can be used to assess the efficacy of thrombolytic therapy. As a noninvasive alternative to pulmonary artery catheterization, we investigated the efficacy of continuous monitoring of end-tidal CO2 tension. DESIGN: In 12 patients with massive pulmonary embolism who required mechanical ventilation, mean pulmonary arterial pressure (MPAP) and end-tidal carbon dioxide tension (ETCO2) were registered continuously during thrombolytic therapy. PaCO2, cardiac index as estimated by thermodilution catheter and respiratory ratio of arterial oxygen tension and inhaled oxygen concentration (PaO2/FIO2) were determined every 60 mins. MEASUREMENTS AND MAIN RESULTS: Before thrombolysis, MPAP (34.5+/-9.8 mm Hg) and the difference between PaCO2 and ETCO2 (10.1+/-4.7 mm Hg) were markedly increased compared with normal values. Continuously monitored MPAP was related to ETCO2 for both all patients (r2 = .42; p < .001) and individually (mean r2 = .92; range, .79-.98; p < .001). In ten survivors, the mean cardiac index and PaO2/FIO2 increased during therapy from 1.7+/-0.4 to 2.8+/-0.6 L/min x m2 and 125+/-27 to 285+/-50 mm Hg (p < .01, respectively). In these patients, the difference between PaCO2 and ETCO2 decreased from 9.8+/-4.5 to 2.8+/-0.9 mm Hg (p < .001). Recurrent embolism was detected in two patients by sudden reduction of ETCO2. CONCLUSIONS: Analysis of ETCO2 allows monitoring of the efficacy of thrombolysis and may reflect recurrent embolism. Thus, on the basis of this small study, analysis of ETCO2 appears to be useful for noninvasive monitoring in mechanically ventilated patients with massive pulmonary embolism.
Acute Disease↗
Soluble L-selectin and neutrophil derived oxidative stress after pacing induced myocardial ischemia in chronic stable coronary artery disease.
We studied the effect of atrial pacing induced myocardial ischemia on levels of soluble L-selectin (sL-selectin) and generation of neutrophil derived reactive oxygen species (ROS) in 10 patients with coronary artery disease (CAD) and stable angina and in six individuals without CAD. Myocardial ischemia was measured metabolically by lactate sampling from the coronary sinus (CS) and arterial blood at each pacing step. Before each pacing step, at peak pacing and shortly after cessation, plasma concentrations of sL-selectin and generation of ROS using the chemiluminescence method were measured in CS and femoral artery blood. Baseline sL-selectin levels in CS samples were significantly lower in the CAD compared to the control group (547 +/- 80 vs 836 +/- 82 ng/mL, P = 0.03). At peak pacing, nine of ten patients with CAD developed myocardial ischemia (lactate extraction ratio at rest 28% +/- 7%, at peak pacing -16% +/- 6%). In these patients, luminol-enhanced chemiluminescence (CL, 0.88 +/- 0.45 vs 1.9 +/- 0.9 cpm x 10(5), P = 0.09) and levels of sL-selectin (547 +/- 80 vs 764 +/- 86 ng/mL, P = 0.03) from naive neutrophils increased significantly in CS blood suggesting a potent in vivo activation of neutrophils. In control patients, incremental pacing caused neither myocardial ischemia nor a significant change of chemiluminescence or of sL-selectin levels. In conclusion, myocardial ischemia induced by pacing tachycardia is able to activate neutrophils in patients with chronic stable coronary artery disease leading to increased generation of ROS and shedding of L-selectin into the coronary circulation.
Adult↗
Cardiac troponin T levels at 96 hours reflect myocardial infarct size: a pathoanatomical study.
We determined the utility of single-point measurements of circulating cardiac troponin T (cTnT) for the noninvasive estimation of infarct size in 16 beagle dogs after left anterior descending artery (LAD) ligation. Pathoanatomical infarct sizes were determined by the triphenyltetrazolium chloride method and correlated with serum concentration changes of cTnT. Peak cTnT levels (14.10 +/- 4.71 microg/l) were reached after 110 +/- 21 h. A significant correlation was found between peak cTnT levels (p = 0.0001, r = 0. 83) or cumulative cTnT levels and relative infarct size (p = 0.0010, r = 0.72). A single cTnT measurement 96 h after LAD ligation was equally predictive of infarct size (p = 0.0010, r = 0.74) as peak or cumulative cTnT levels derived from serial sampling. cTnT levels at 96 h may thus be useful for practical and cost-effective estimation of infarct size.
Animals↗