Platelet microparticles and calcium homeostasis in acute coronary ischemias.

UNLABELLED: Elevation of free cytoplasmic calcium is the common pathway of platelet activation, leading to shape change, shedding of platelet microparticles (PMP), aggregation, and secretion of internal granules, including expression of CD62p on the surface. Platelet activation is well documented in unstable angina (UA) and acute myocardial infarction (MI). We investigated the following markers of platelet activation in 55 patients undergoing coronary angiography for suspected CAD: free cytoplasmic calcium, [Ca2+]cyt, PMP, CD62p expression, and platelet/leukocyte (P/L) interaction. [Ca2+]cyt was measured by Fluo-3 and the other measurements were by flow cytometry. Patients were classified into three groups: unstable angina (UA, n = 11), recent myocardial infarction (MI, n = 11), and patient controls (CTL, n = 33). Blood was drawn before infusion of heparin through femoral lines at the time of catheterizaton for assays. ( RESULTS: (1) PMP values were significantly higher in both UA and MI than in CTL, P < 0.05. There was no difference between UA and MI. (2) P/L interaction was significantly elevated only in UA, P < 0.05. (3) CD62p expression on free platelets did not differ significantly between any of the three groups. (4) The resting [Ca2+]cyt, thrombin-induced Ca2+ influx, and release of Ca2+ from internal stores were all significantly higher in platelets from the combined patient group (UA + MI) than in the patient control group, P < 0.001 CONCLUSIONS: Results on calcium hemostasis and PMP were significantly different in patients with acute coronary syndromes than those with stable angina or no coronary ischemia; this may reflect underlying pathophysiology of acute coronary ischemia. P/L interaction was higher only in the UA group, suggesting a role of leukocytes in UA.

Effects of intracoronary carbon dioxide on left ventricular function in swine.

BACKGROUND AND HYPOTHESIS: Carbon dioxide is currently used as an arterial and venous contrast agent; however, little is known of its effects on left ventricular function. This study was undertaken to investigate those effects. METHODS: Ascending doses of 5, 10, and 20 ml of carbon dioxide were administered into the left main coronary artery of domestic swine with and without a continuous infusion of intravenous nitroglycerin (50 micrograms/min). RESULTS: Carbon dioxide had an immediate and profound depressant effect on both systolic and diastolic left ventricular function associated with ischemic electrocardiographic changes. Compared with controls (% change), ascending doses of carbon dioxide decreased systolic pressure by -35 +/- 7, -48 +/- 8, and -53 +/- 4 in the absence of nitroglycerin, and by -32 +/- 9, -50 +/- 9, and -60 +/- 9 in the presence of nitroglycerin. Peak+dP/dt decreased by -54 +/- 7, -61 +/- 11, and -64 +/- 3 in the absence of nitroglycerin, and by -36 +/- 13, -55 +/- 11, and -65 +/- 11 in the presence of nitroglycerin. Minimum -dP/dt increased by 65 +/- 8,71 +/- 8, and 77 +/- 3 in the absence of nitroglycerin, and by 63 +/- 7,71 +/- 8, and 78 +/- 7 in the presence of nitroglycerin. No significant changes in heart rate were observed; however, widespread ST-segment elevation was observed in all animals. Coronary angiography following carbon dioxide injection revealed a marked decrease in coronary flow velocity until the gas was cleared from the microcirculation. This was also documented by direct measurement of flow velocity using a Doppler catheter in an additional animal. Left ventriculography demonstrated immediate global dilation and depression of systolic function. CONCLUSIONS: In the swine model, relatively small doses of intracoronary carbon dioxide cause profound yet reversible global left ventricular dysfunction which appears to be ischemic in origin.

ST segment tracking for rapid determination of patency of the infarct-related artery in acute myocardial infarction.

OBJECTIVES: This study was designed to test the hypothesis that monitoring the ST segment on a single electrocardiographic (ECG) lead reflecting activity in the infarct zone provides sensitive and specific recognition of reperfusion within 60 min of initiation of therapy in acute myocardial infarction. BACKGROUND: Infarct-related arteries that fail to recanalize early may benefit from immediate rescue angioplasty. Hence, detection of reperfusion has important practical clinical implications. METHODS: Of 41 patients with acute myocardial infarction who had ambulatory ECG (Holter) monitors placed, 38 had adequate ST segment monitoring for 3 h; 35 of the 38 were treated with thrombolytic agents and 3 with primary angioplasty. All patients underwent early coronary angiography and were classified into two groups: Group P (22 patients) had angiographic patency (Thrombolysis in Myocardial Infarction [TIMI] grade 2 or 3 flow), the Group O (16 patients) had persistent occlusion (TIMI grade 0 or 1 flow) of the infarct-related vessel at 60 min from initiation of therapy. The initial ST segment level was defined as the first ST segment level recorded; the peak ST segment level was defined as the highest ST segment level measured during the 1st 60 min. To assess the optimal ST segment recovery criteria for reperfusion, the presence or absence of a > or = 75%, > or = 50% and > or = 25% decrement from initial and peak ST segment levels, sampled and analyzed at 2.5-, 5-, 10-, 15-and 20-min intervals, was correlated with patency of the infarct-related artery at 60 min. RESULTS: ST segment recovery of > or = 50% reduction from peak ST segment levels with sampling rates at < or = 10-min intervals provided the optimal criterion for recognizing coronary artery patency at 60 min (sensitivity 96%, 95% confidence interval [CI] 77% to 99%; specificity 94%, 95% CI 69% to 99%, p < 0.0001). The subgroup of 13 patients in Group P with TIMI grade 3 reperfusion flow all met this criterion (sensitivity 100%, 95% CI 75% to 100%). The use of the initial ST segment level as the baseline for determining the presence of a > or = 50% reduction in ST segment levels within 60 min was less sensitive. Prediction of coronary reperfusion within 60 min of therapy on the basis of a > or = 75% decrement from peak ST segment levels was less sensitive, and the use of a > or = 25% decrement was less specific. CONCLUSIONS: ST segment monitoring of a single lead reflecting the infarct zone provides a reliable method for assessing reperfusion within 60 min of acute myocardial infarction. Optimal criteria for ECG reperfusion include a > or = 50% decrease from peak ST segment levels, with ST segment measurements recorded continuously or at least every 10 min.

Comparisons of paired orthotopic cardiac transplant donor and recipient electrocardiograms.

Electrocardiograms of 20 consecutive donor and paired recipient orthotopic heart transplant patients were compared. Recipients were markedly older than donors; all patients were males, and both groups had similar body weight. The heart rate was faster, QRS was longer, QT was shorter, QRS axis was more shift to the left, and precordial voltage was decreased in the recipient ECGs in the first 72 hours after transplant. These changes persisted during late follow-up (12 +/- 6 months after transplant). Seventy percent and 60% of recipients within the first 72 hours after transplant and during late follow-up, respectively, had a new RBBB delay compared to their paired donor ECG. There was a trend toward less clockwise rotation in the ECGs of patients who had a new incomplete RBBB in the late follow-up compared to patients who did not. Thus new RBBB delays, QT shortening, QRS axis left shift, and decrease in precordial voltage are commonly seen on ECGs after orthotopic cardiac transplantation. A new heart position and recipient's weight do not seem to account for the development of a new RBBB delay and decrease in precordial voltage. Other factors, such as mechanical or thermal injury and change in donor-to-recipient age, may be involved.

Effectiveness of holmium laser-assisted coronary angioplasty. The Holmium Laser Coronary Registry.

The efficacy of holmium laser-assisted angioplasty was studied in 365 narrowings in 331 consecutive patients with coronary artery disease. Clinical indications for study were unstable angina pectoris in 140 patients (42%), stable angina in 136 patients (41%), postmyocardial infarction angina in 35 patients (10.5%), silent myocardial ischemia in 11 patients (3%), acute myocardial infarction in 1 patient (0.3%) and undefined in 8 patients (2%). Coronary morphology characteristics by Multivessel Angioplasty Prognosis Study group criteria were type A in 12.6%, type B1 in 34.2%, type B2 in 27.4% and type C in 25.4%. The laser successfully crossed the total length of the narrowing in 85.2%. Procedural success was 94.2%. Laser alone reduced mean percent luminal narrowing from 88 +/- 11% to 57 +/- 22%. Subsequent balloon angioplasty further reduced the mean luminal narrowing to 23 +/- 18%. Major complication rate was 2.7% (death 0.3%, Q-wave myocardial infarction 0.5%, and emergent bypass surgery 2.7%). Six-month angiographic restenosis (> 50% stenosis) rate was 44%.

Intraaortic balloon entrapment.

A review of intraaortic balloon pump use at the University of Miami/Jackson Memorial Medical Center over the past 21 years identified 2 cases where a balloon was found to be entrapped. The balloon catheters had been in place for approximately 10 days when this complication occurred. The retained balloons were torn, filled with clotted blood, and impacted in the vasculature. In our first case, forceful removal of the intraaortic balloon was complicated by unintentional extraction of the external iliac and common femoral arteries. In the second case, clot within the balloon was dissolved with tissue plasminogen activator injected into the drive lumen of the catheter before removal. The prevention and management of this rare but serious complication of intraaortic balloon pumping is reviewed.

Pulmonary edema associated with electrical injury.

The occurrence of cardiogenic pulmonary edema following alternating current electrical injury has not been reported. A patient developing severe pulmonary edema immediately following an electrical injury-induced episode of ventricular fibrillation is described. Evidence that the etiology of the pulmonary edema was cardiogenic is derived from both hemodynamic data and the calculation of the pulmonary edema fluid to serum colloid osmotic pressure ratio.

Interrelationship of variable coupling, multiformity and repetitive forms: implications for classification of ventricular arrhythmias.

One hundred 24-hour ambulatory electrocardiograms were prospectively examined to determine the relationship of variable coupling and multiformity of single premature ventricular complexes to repetitive forms. Premature ventricular complexes were present in 86 patients and were categorized by a three-tier decision-making tree using (1) multiformity confirmed in two channels, (2) variable coupling of greater than 80 msec of premature ventricular complexes of similar QRS morphologies, and (3) repetitive forms of greater than or equal to 2 premature ventricular complexes. Variable coupling was present in 51 patients, among whom 35 (69%) had repetitive forms; multiformity was present in 46 patients, among whom 37 (80%) had repetitive forms; repetitive forms were present in 41 patients, among whom only one patient (2%) did not demonstrate multiformity or variable coupling. Variable coupling, multiformity, or either were significantly associated with the occurrence of repetitive forms (chi square = 34, 15, 29, respectively, each p less than 0.005). There was a bimodal distribution between patients with uniform, fixed coupled premature ventricular complexes who had rare repetitive forms (1 of 26) and patients with multiformity and variable coupling of premature ventricular complexes who had significantly more repetitive forms (30 of 37; p less than 0.001). The frequency distribution of repetitive form length suggested a natural break point between five and six consecutive complexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Compression of an anomalous left circumflex coronary artery by a bioprosthetic valve ring.

The most common anomaly of the coronary arteries is the origin of the left circumflex artery from the right sinus of Valsalva or the right coronary artery proper. This anomaly is rarely clinically significant. A patient is reported here who has such an anomaly which did become clinically significant after a bioprosthetic aortic valve replacement. The circumflex artery described here became compressed between the Hancock aortic valvular ring and the mitral valvular apparatus. This case is the first antemortem report of such a compression to be demonstrated angiographically and the first case to be the results of an aortic bioprosthetic ring alone. Special surgical considerations must be made when performing valvular replacements on patients with this coronary artery anomaly.

Angiographic demonstration of atherosclerotic stenosis, arterial spasm, and thrombus formation in an infarct-related coronary artery.

Clinical, angiographic, and pathologic data support the contention that atherosclerosis, platelet aggregation, and coronary vasomotility work in unison to cause coronary thrombosis, which in turn leads to myocardial infarction. A patient is described in whom, 2 months after an acute myocardial infarction, inducible coronary artery spasm and a nonocclusive thrombus were angiographically demonstrated at the site of a minimal atherosclerotic narrowing in the infarction-related vessel. This report, to the best of our knowledge, is the first time that these three pathophysiologic mechanisms have been shown, in vivo, to be occurring concomitantly in an infarct-related vessel. Documentation of the unified occurrence of these phenomena support the current concept of the pathophysiology of myocardial infarction.