Molecular markers relevant to myocardial injury following dental extraction in patients with or without coronary artery disease.

OBJECTIVES: The aim of this study was to characterize biological changes following dental extractions in patients with or without coronary artery disease (CAD). MATERIALS AND METHODS: Forty-five patients (36 males and 9 females) referred for dental extraction underwent treatment and provided blood samples before, immediately after, and 24 h after the procedure. A broad array of biomarkers was employed to assess myocardial injury (highly sensitive troponin T, hs-TnT), bacterial burden (LPS endotoxin activity), and systemic inflammation (CRP, fibrinogen, IFN-γ, IL-1ß, IL-6, IL-8, IL-10, IL-12, and TNF-α). RESULTS: Dental extraction in patients with or without CAD was associated with rises in hs-TnT (p = 0.013), hs-CRP (p < 0.001), fibrinogen (p = 0.005), endotoxin activity (p < 0.001), IFN-γ (p < 0.001), IL-6 (p < 0.001), IL-8 (p = 0.011), and IL-12 (p < 0.001) at 24 h compared with immediately post procedure. Changes in systemic inflammation and endotoxin activity were more evident in those with hs-TnT rise. CONCLUSIONS: Simple dental extractions may cause mild increase in hs-TnT, indicating minor myocardial injury in both patients with or without CAD. Acute systemic inflammation and endotoxemia could represent a possible link between invasive dental treatment and increased risk of acute cardiovascular events. These findings indicate that invasive dental treatment (as simple as a single dental extraction) may impact negatively on clinical outcomes in dental patients, especially those with CAD.

Minor myocardial injury after elective uncomplicated successful PTCA with or without stenting: detection by cardiac troponins.

Cardiac troponins are sensitive and specific markers for the detection of minor myocardial injury. However, they have been rarely used to monitor myocardial injury after coronary stenting. The purpose of the study was to measure cardiac troponin I (cTnI) and cardiac troponin T (cTnT) levels after elective uncomplicated successful percutaneous transluminal coronary angioplasty (PTCA) with or without coronary stenting and to compare their results with serum creatinine kinase MB isoenzyme (CKMB). CTnI and cTnT levels were compared with those of CK or CKMB in 98 consecutive patients with stable angina undergoing elective uncomplicated successful PTCA with stenting (n = 71) or without stenting (n = 27). Markers were measured before and 6, 12, 24, and 48 hr after the procedure. Peak postprocedural levels for each marker were compared and related to angiographic and procedural characteristics as well as to the occurrence of side-branch occlusion. None of the patients had abnormal markers before the procedure. Abnormal postprocedural values of one or more markers were observed in 28 patients (29%), 23 after stenting and 5 after PTCA alone. The frequencies of abnormal cTnI and cTnT levels were significantly higher than that of CKMB after coronary intervention (26% and 18% vs. 7%; P = 0.00016 and 0.015, respectively), with cTnI being the most significant. When compared with troponin-negative patients, abnormal cardiac troponin values were significantly related to total time of inflation (223 +/- 128 vs. 170 +/- 105 sec; P = 0.008) and inflation maximal pressure (12.9 +/- 2.3 vs. 12.0 +/- 2.7 atm; P = 0.04). Small side-branch occlusion was noticed in 36% of the troponin-positive patients and in 6% of the troponin-negative group (P = 0.00047). In conclusion, minor myocardial injury is not uncommon after elective uncomplicated successful PTCA with or without stenting. Cardiac troponins, especially cTnI, are more sensitive than CKMB for the detection of this minor myocardial injury. Total time of inflation and inflation maximal pressure are predictors of postprocedural elevation of cardiac troponins. Side-branch occlusion may account for some, but not all, periprocedural minor myocardial injury.

Detection of minor myocardial injury after successful percutaneous transluminal coronary angioplasty with or without stenting.

Cardiac troponins are sensitive and specific markers for the detection of minor myocardial injury. However, they have been rarely used to monitor myocardial injury after coronary stenting. The purpose of the study was to measure cardiac troponin I (cTnI) and cardiac troponin T (cTnT) levels after apparently successful percutaneous transluminal coronary angioplasty (PTCA) with or without coronary stenting and to compare their results with serum creatine kinase (CK) and its isoform, creatine kinase-MB (CKMB). CTnI and cTnT levels were compared with those of CK or CKMB in 50 consecutive patients with stable angina undergoing visually successful PTCA with stenting (n = 35) or without stenting (n = 15). Cardiac TnI, cTnT, CK and CKMB levels were measured before and 6, 24, and 48 hours after the procedures was performed. None of the patients had abnormal cTnI or cTnT levels, CK activity, or CKMB levels before the procedures. Moreover, no patient showed electrocardiographic evidence of myocardial infarction. 13 patients (26%) had abnormal peak values of one or more markers at 24 hours after coronary intervention. Troponin I was elevated in 10/35 patients after coronary stenting (29%) and in 2/15 patients after PTCA (13%) (P = 0.327). Troponin T was elevated in 6 patients (17%) and CKMB activity was elevated in 3 patients (9%) of the coronary stenting group. CTnI was more significant than CKMB (P = 0.023) in detecting minor myocardial injury. When compared with cTnI and CKMB, cTnT did not reach significance (P = 0.129 and 0.489, respectively). 5 out of the 13 patients with abnormal markers (38%) developed side branch occlusion after stenting. In conclusion, cTnI was a very sensitive marker in detecting minor myocardial injury after coronary angioplasty with or without stenting. The frequency of increased serum levels of cardiac troponins was higher in patients undergoing stent implantation than in those treated with angioplasty alone but did not reach significance. Side branch occlusion may have accounted for some, but not all, periprocedural minor myocardial injury in the stent group.

Cardiac markers for assessing the acute coronary syndromes. A focus on cardiac troponins.

Markers of myocardial injury will continue to play an essential role in the assessment and management of patients presenting within the spectrum of acute coronary syndromes, a term representing the continuum of acute myocardial ischemia ranging from angina through Q-wave myocardial infarction. Coronary artery lesion instability can be detected by markers of plaque inflammation and disruption, platelets reactivity, and thrombosis. When myocardial injury occurs with severe impairment of coronary blood flow, several markers are released from the damaged myocyte. For many years, creatine kinase-MB isoenzyme has been the conventional marker for myocardial infarction. Despite its inadequate sensitivity and specificity for myocardial injury, creatine kinase-MB remains an essential component in assessing re-infarction or infarct extension, as well as in monitoring reperfusion after thrombolytic therapy when combined with myoglobin. Among the many cardiac markers for myocardial necrosis, cardiac troponins possess superior sensitivity and specificity for the detection of myocardial injury. In addition to their superior performance in detecting minor myocardial damage, cardiac troponins can be useful in detecting perioperative myocardial infarction, infarct size, improving risk stratification, and facilitating therapeutic decision making in patients with acute coronary syndromes.

Cardiac markers used in the detection of myocardial injury.

OBJECTIVE: Activities of total creatine kinase and its isoform creatine kinase are usually significantly elevated in patients with myocardial or skeletal muscle injury as well as in those with renal failure. The purpose of this study was to compare findings for creatine kinase mass, cardiac troponin T and cardiac troponin I with those of creatine kinase and creatine kinase MB activity. METHODS: Blood samples from 118 patients were studied. Fifty eight patients had significantly elevated creatine kinase activity (39 with and 19 without clinically proven myocardial injury or infarction) and 60 were normal controls. The sensitivity, specificity, positive and negative predictive values were calculated for all markers. RESULTS: Cardiac troponins had 100% sensitivity and negative predictive value, for myocardial injury, as compared with 92% and 96% for creatine kinase activity and 96% and 97% for creatine kinase-mass. Cardiac TnI had the highest specificity and positive predictive value (99% and 98%) as compared with cardiac troponin T (96% and 93%), creatine kinase-mass (92% and 86%) and creatine kinase activity (89% and 80%). CONCLUSION: Cardiac troponins, especially cardiac troponin T, have very high sensitivity, specificity and predictive value for myocardial injury.

Diffuse thallium lung uptake in Pneumocystis carinii pneumonia.

Five patients with AIDS with Pneumocystis carinii pneumonia (PCP) showed diffuse bilateral lung uptake on sequential thallium and gallium scans. This creates a problem in the sequential use of these tests for the differentiation of Kaposi's sarcoma from acute inflammatory or other malignant diseases. In Kaposi's sarcoma, thallium uptake is usually focal and not diffuse unless associated with other pathology. However, in PCP the diffuse thallium lung uptake may be due to congestion, increased vascular permeability, and extravasation of thallium into the lung parenchyma.

Idiopathic long QT syndrome: asking the right question.

Infants and young children cannot describe symptoms of cardiogenic syncope accurately. If the attention in such cases is focused on the seizure activity that may follow, the patient will be treated inappropriately with anticonvulsants. We report such a presentation in 4 infants and young children (ages 6 to 48 months) with idiopathic long QT syndrome. All patients presented with recurrent seizures. All patients had a corrected QT interval (QTc) > or = 0.44 s and none had deafness. The diagnosis was suspected by careful history-taking which revealed episodes of loss of consciousness before convulsions in all patients. All patients were treated successfully with propranolol and remained free of symptoms during the follow-up period of 1-2 years. Screening the other family members revealed a prolonged QTc in 9 out of 16, and a history of 3 sudden and unexplained deaths in two families.

Recordings from the slow zone of reentry during burst pacing versus programmed premature stimulation for initiation of reentrant ventricular tachycardia in patients with coronary artery disease.

Programmed premature stimulation and burst pacing were compared for initiation of ventricular tachycardia (VT) in 16 patients with inducible sustained monomorphic VT. In all patients VT could be induced by programmed stimulation with 2 or 3 extrastimuli. On the other hand, initiation of VT by burst pacing was dependent on the length of the train; only 2 to 4 of the 11 trains tested could induce VT in any single patient. Recordings obtained from the slow zone of reentry showed that programmed premature stimulation that induced VT resulted in a critical degree of conduction delay as revealed by lengthening of local fractionated electrograms spanning 70 to 100% of the diastolic interval. Similarly, the last beat of a burst pacing train that induced VT was always followed by a similar degree of local conduction delay, whereas trains that failed to induce VT were followed by a lesser delay. It is concluded that although programmed stimulation with up to 3 extrastimuli was consistently successful in inducing VT, burst pacing succeeded in only 26% of the trials and was dependent on the length of the train, which varied from one patient to the other. Similar to what was shown previously in the experimental model of reentrant VT, burst pacing could initiate, conceal, terminate, and reinitiate reentry depending on the length of the train.

TU alternans, long QTU, and torsade de pointes: clinical and experimental observations.

T or U wave alternans in association with long QTU and torsade de pointes (TdP) is uncommon and its mechanism(s) is unknown. We studied three patients with TU alternans, long QTU, and TdP: patient 1 was a newborn with congenital long QTU; patient 2 had marked hypokalemia and hypomagnesemia; and patient 3 was receiving procainamide. In the three patients, TU alternans was tachycardia dependent and preceded the onset of TdP. In the patient on procainamide, TU alternans and TdP occurred at long cardiac cycles. In this patient, endocardial monophasic action potential (MAP) recordings showed that TU alternans was associated with alternation of the duration of the plateau. A deflection consistent with early afterdepolarization (EAD) arose at a constant time interval from phase 0 but alternated from high and low levels of phase 3. The first ectopic beat of TdP arose on the descending limb of the EAD. TU alternans was investigated by MAP recordings in six normal dogs, following the administration of anthopleurin-A (AP-A), a drug shown to delay sodium inactivation and to induce bradycardia dependent long QTU, EADs, and TdP. In two dogs TU alternans was associated with 2:1 recordings of EAD and nearly constant plateau duration. In three dogs, TU alternans was associated with EAD that occurred in consecutive beats at constant time intervals from phase 0, but alternated from high and low phase 3 because of alternation of the duration of the plateau. In one dog, alternation of EAD and plateau duration occurred. In 36 separate episodes of TdP that were analyzed in the six dogs, 32 were bradycardia dependent but four developed on abrupt shortening of the cardiac cycle associated with alternation of action potential duration. Our results suggest: (1) TU alternans may be due to 2:1 propagation of an EAD or to alternation of the recovery kinetics of a repolarization current; (2) The constant occurrence of EAD in relation to phase 0 in spite of alternation of plateau duration suggests an ionic mechanism synchronized to depolarization; (3) Tachycardia dependent TdP in clinical and experimental examples of long QTU seems to be characteristically associated with TU alternans. Dispersion of repolarization may underlie the increased ventricular electrical instability in these cases.

Left atrial systolic antegrade flow in patients with mitral regurgitation: a pulsed Doppler sign displayed by color flow imaging.

Twenty-two patients with severe mitral regurgitation were observed to have turbulent systolic antegrade flow on pulsed Doppler mapping of the left atrium. All were studied by color flow imaging to delineate the mechanism of this peculiar flow. Pulsed Doppler findings of an eccentric regurgitant flow in one side, an antegrade systolic flow with slightly delayed onset in the other side, and a low velocity flow near the posterior wall, were consistant with the theory of a large eccentric regurgitant jet swirling in the left atrium. Color flow imaging confirmed this mechanism in all patients. Nineteen patients had flail mitral valve with a positive predictive value of 86%. The other three patients had deformed rheumatic mitral valve. The severity of mitral regurgitation was confirmed in all 16 patients studied by left ventricular cineangiography. We have shown that the antegrade systolic left atrial flow is the result of the swirling of a large regurgitant eccentric jet, is commonly observed with flail mitral valve, can occur in patients with deformed rheumatic mitral valve without flail leaflet, and most significantly indicates the presence of severe mitral regurgitation.

Valve surgery in acute rheumatic heart disease. One- to four-year follow-up.

Six patients with acute rheumatic carditis and intractable left ventricular failure, all in class 4 NYHA classification, underwent successful valve surgery combined with medical therapy. Two-dimensional echocardiography and Doppler studies showed all of them to have left ventricular dilatation, with good systolic function, together with severe mitral regurgitation; two patients also had severe aortic regurgitation. Over a mean follow-up period of two years, no mortality was recorded, and all six patients were in NYHA class 1-2. We conclude that valve replacement is not contraindicated in acute rheumatic carditis and may be preferable to repair.

Traumatic papillary muscle dysfunction: attempted mitral-valve repair and eventual prosthetic replacement.

A previously healthy young man sustained a deceleration chest injury. Severe mitral regurgitation was confirmed by Doppler and cardiac catheterisation. The mitral valve and subvalvular apparatus appeared normal at the subsequent surgery. Papillary muscle dysfunction was considered to be the principal cause of the regurgitation. Mitral-valve repair failed to preserve the competence of the valve, leading to successful mitral-valve replacement. Histology of the papillary muscle showed necrosis, confirming the original diagnosis. Post-traumatic papillary muscle dysfunction is concluded to be one of the cause of severe mitral regurgitation. Appropriate treatment is valve replacement rather than attempting conservative management.

Heparin resistance induced by intravenous nitroglycerin. A word of caution when both drugs are used concomitantly.

Intravenous (IV) nitroglycerin was found to interfere with the anticoagulant effect of heparin during eight infusions of both drugs in seven patients who were closely monitored with frequent activated partial thromboplastin time determinations. All patients were resistant to heparin when receiving IV nitroglycerin and had a marked increase in sensitivity when discontinuing the IV nitroglycerin therapy. This effect was present whether or not propylene glycol was in the preparation. Patients treated with simultaneous IV nitroglycerin and IV heparin must be monitored often to avoid inadequate anticoagulation, and heparin dosage should be decreased when stopping IV nitroglycerin therapy to avoid hemorrhage.