A study to determine chest wall vibratory attachment interface locations for a low frequency sonic vibrator in treatment of acute coronary thrombosis.

Our institution is developing a non-invasive Diastolic Timed Vibrator (DTV) to enhance emergency clearance of acute coronary thrombosis. Sonic frequency diastolic vibro-percussion (i.e. 50 Hz, 2 mm amplitude) applied upon the rib-spaces of the left sternal border has shown to improve left ventricular performance and coronary flow in human volunteers. However, therapeutic acoustic penetrability cannot be assumed depending on varying chest size and lung position which attenuates acoustic transmissions. Furthermore, chest locations enabling a direct lung free pathway overlying the base of the heart (wherein the coronaries arise) should be promoted, while locations overlying the left ventricular apex (site of potential thrombus formation) should be avoided. We therefore set out to determine preferred chest wall placement positions for a vibratory interface suitable for treatment of ST Elevation Myocardial Infarction (STEMI). Inter-Costal Space (ICS) positions to the left or right of the sternum were interrogated in 90 adults following routine Echocardiography to ascertain whether the base of the heart could be imaged (hence inferring acoustic transmissibility), and to determine over what part of the heart each transducer position was overlying. The third and fourth ICS proximate the left sternal border provided acoustic transmissibility in 96 and 100% of cases respectively, with only one unwanted occurrence from the fourth ICS where the transducer overlaid the apical third of the left ventricle. Acoustic transmissibility from third and fourth ICS right sternal border was documented in 53 and 85% of cases respectively. A vibration interface in STEMI treatment should allow for contact overlying the left and right third and fourth ICS generally proximate the sternal borders. As vibration transmission to the cardiac apex and/or left atrium cannot be completely avoided, vibration therapy should be contra-indicated in late presenters for antero-septal apical STEMI, and in cases of new onset atrial fibrillation persisting greater than 48 h which have not been adequately anti-coagulated.

Coronary thrombosis and marijuana smoking: a case report and narrative review of the literature.

We encountered evidence of myocardial infarction due to coronary thrombosis in an autopsy of an occasional marijuana smoker. These findings prompted us to perform a narrative review of the literature to determine when post-mortem toxicological tests may support a temporal relationship between marijuana smoking and cardiovascular disease. Toxicological examination showed the presence of Δ-9-tetrahydrocannabinol, its main metabolite and cannabinol in blood and urine. Quali-quantitative analysis revealed that Δ-9-tetrahydrocannabinol was taken within 2 h of the onset of cardiovascular symptoms, according to circumstantial data. Post-mortem toxicological results must take into account the degradation and post-mortem redistribution of analytes. However, for any inference about the specific cardiovascular triggering effect of Δ-9-tetrahydrocannabinol intake, we maintain that cannabinoid analysis in blood samples must be considered an essential requirement to estimate the time of last intake and avoid incomplete documentation. The literature, combined with the present case report, highlights an association between marijuana use and negative cardiovascular events, although few authors have supported their conclusions with toxicological results. Thus, additional research is needed.

Fibrinopeptide A excretion in urine: a marker of the cumulative thrombin activity in stable versus unstable angina patients.

Plasma levels and 24-hour urine excretion of fibrinopeptide A were measured in a consecutive series of 179 patients with angina pectoris. Sixty-four patients had stable angina and 115 patients had unstable angina. Urine was collected over 24 hours the day before coronary arteriography, and blood samples were taken at the end of urine collection. When the values of fibrinopeptide A in plasma and in the 24-hour urine specimens were compared, no significant correlation was found in patients with either stable (rs = 0.16, difference not significant) and unstable (rs = 0.07, difference not significant) angina. The concentrations of fibrinopeptide A in the plasma did not differ significantly when patients with stable angina (range 0.1 to 82.6, median 7.4 ng/mL) were compared with patients with unstable angina (range 0.2 to 61.7, median 14 ng/mL, p = 0.055), whereas fibrinopeptide A 24-hour urinary excretion was significantly higher in patients with unstable angina (range 0.3 to 38.1, median 11.8 micrograms/24 hr) than in patients with stable angina (range 0.4 to 38.1, median 3.8 micrograms/24 hr, p less than 0.001). Twenty-four-hour urine excretion of fibrinopeptide A in patients with unstable angina and angiographically documented intracoronary thrombi were higher than the corresponding values in patients with unstable angina without such angiographic characteristic (p less than 0.001). The largest increase in plasma and urine concentration of fibrinopeptide A was observed in patients whose first episode of angina at rest occurred within the previous 48 hours. We conclude that the cumulative thrombin activity, assessed by 24-hour urinary excretion of fibrinopeptide A, is a more useful index, compared with single fibrinopeptide A measurement in plasma, for discriminating between patients with stable and with unstable angina pectoris.

Coronary artery thrombosis and elevated urine immunoreactive thromboxane B2.

Immunoreactive thromboxane B2 (i-TXB2) was measured by radio-immunoassay (RIA) in urines collected over eight hours on the day of admission in 25 patients who were admitted with the diagnosis of myocardial infarction. In 16 of the patients myocardial infarction was confirmed by ECG and plasma enzymes. Another patient presented with pulmonary embolism and the remaining eight patients had angina pectoris. A further eight hour urine collection was obtained 24 hours later from eleven of the sixteen patients with myocardial infarction. In these eleven patients myocardial infarction was associated with five fold higher urine i-TXB2 (2.72 +/- 0.48 ng/ml) at the day of admission when compared to patients admitted under the same diagnosis but found to have angina only (0.51 +/- 0.08 ng/ml, p less than 0.001). In patients with myocardial infarction the urine i-TXB2 values were reduced 24 hours later (1.58 +/- 0.27 ng/ml, p less than 0.01). One patient was followed with urine i-TXB2 from three days prior to diagnosis of myocardial infarction and to one day prior to a second infarction. In this patient i-TXB2 was highest three days prior to infarction. We conclude that this early elevation of urine i-TXB2 three days prior to diagnosis of infarction and the increased i-TXB2 in patients with myocardial infarction when compared to patients with angina suggest thromboxane is probably released from activated platelets prior to infarction. We suggest that urine i-TXB2 may be of value in the differential diagnosis between myocardial infarction and angina.