Enhanced metaboreflex sensitivity in hypertensive humans.

The exercise pressor reflex (EPR) is composed of the mechanoreflex and the metaboreflex and has been shown to be overactive in spontaneously hypertensive rats. The aim of the present study was to isolate the metaboreflex using post-exercise ischemia (PEI) and examine the BP response in normotensive (NTN) and hypertensive (HTN) humans. We hypothesize that the post-exercise ischemia-induced maintenance of BP will be greater in HTN when compared to NTN adults. A total of 15 NTN (65 +/- 1 years) and 12 HTN (64 +/- 1 years) adults were recruited. Beat-to-beat mean arterial pressure (MAP) was measured non-invasively (Finometer). Dynamic handgrip exercise (DHE) was performed for 3 min followed by 2 min of PEI. An unpaired t test was used to examine differences between groups. As compared to resting baseline values, the change in MAP during PEI was greater in HTN than NTN subjects (HTN: Delta = 12 +/- 3 mmHg, NTN: Delta = 6 +/- 1 mmHg, P < 0.05). These data suggest that HTN humans have enhanced metaboreflex sensitivity.

An evaluation of serum troponin T and signal-averaged electrocardiography in predicting electrocardiographic abnormalities after blunt chest trauma.

OBJECTIVE: Despite multiple inquiries, there are no available tests to definitively detect blunt myocardial injury. The evaluation of patients with chest wall injuries without other indications for intensive care unit (ICU) admission has ranged from a single emergency department electrocardiogram (ECG) to 72 hours of continuous electrocardiographic monitoring. Recently, signal-averaged ECG and serum cardiac troponin T have demonstrated clinical utility in the evaluation of ischemic heart disease. The purpose of this study is to determine the ability of these diagnostic tests to predict the occurrence of significant electrocardiographic rhythm disturbances for patients with chest wall injuries and no other indication for ICU admission. METHODS: We prospectively evaluated 71 consecutive adult patients admitted to a regional Level I trauma center with chest wall injuries not requiring ICU admission. We obtained admission signal-averaged ECG, serum troponin T level, standard ECG, and creatine phosphokinase (CPK-MB) level. Patients received continuous electrocardiographic monitoring, follow-up 12-lead electrocardiography, and serial monitoring of troponin and CPK-MB. Echocardiography was performed for patients with abnormal CPK-MB levels. Electrocardiographic events were graded as normal, abnormal but clinically insignificant, or clinically significant. Multiple stepwise logistic regression analysis was used to evaluate predictors for the development of clinically significant electrocardiographic events. RESULTS: On admission, 17 of 71 patients (23.9%) had normal sinus rhythm; 13 (18.3%) had a clinically significant finding. For 50 patients, follow-up ECG was abnormal; for 26, the findings were clinically significant. Of 17 patients with normal initial ECGs, 7 (41%) developed a clinically significant abnormality. Six patients received intervention for ECG findings. Eleven of 71 patients (16%) had positive troponin T; 5 of 71 (7%) had positive CPK-MB; 15 of 71 (21%) had positive signal-averaged ECG; and 4 of 13 had positive echocardiograms. Initial electrocardiographic abnormalities and a troponin T level > 0.20 microg/L were the only variables found to predict clinically significant electrocardiographic events. Sensitivity and specificity of troponin T in predicting clinically significant abnormalities were 27 and 91%, respectively. CONCLUSIONS: 1. The best predictors for the development of significant electrocardiographic changes are an admission ECG abnormality and an elevated serum troponin T level. 2. Both tests have high specificity with low to moderate sensitivity. 3. Patients with normal ECGs may develop clinically significant events. 4. CPK-MB and echocardiograms continue to be poor predictors of significant electrocardiographic events.

Beneficial effects of cholesterol-lowering therapy on the coronary endothelium in patients with coronary artery disease.

BACKGROUND: Impaired endothelium-mediated relaxation contributes to vasospasm and myocardial ischemia in patients with coronary artery disease. We hypothesized that cholesterol-lowering therapy with the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor lovastatin could improve endothelium-mediated responses in patients with coronary atherosclerosis. METHODS: In a randomized, double-blind, placebo-controlled trial, we studied coronary endothelial responses in 23 patients randomly assigned to either lovastatin (40 mg twice daily; 11 patients) or placebo (12 patients) plus a lipid-lowering diet (American Heart Association Step 1 diet). Patients were studied 12 days after randomization and again at 5 1/2 months. These patients had total cholesterol levels ranging from 160 to 300 mg per deciliter (4.1 to 7.8 mmol per liter) and were undergoing coronary angioplasty. At the initial and follow-up studies, patients received serial intracoronary infusions (in a coronary artery not undergoing angioplasty) of acetylcholine to assess endothelium-mediated vasodilatation. The responses of the coronary vessels were analyzed with quantitative angiography. RESULTS: The patients in the placebo and lovastatin groups had similar responses to acetylcholine at a mean of 12 days of therapy (expressed as the percentage of change in diameter in response to acetylcholine doses of 10(-9) M, 10(-8) M, 10(-7) M, and 10(-6) M). In the placebo group, the respective mean (+/- SE) changes were 1 +/- 2, 0 +/- 2, -2 +/- 4, and -19 +/- 4 percent; in the lovastatin group, they were -2 +/- 2, -4 +/- 4, -12 +/- 5, and -16 +/- 7 percent (P = 0.32). (Coronary-artery constriction is reflected by negative numbers). The responses to acetylcholine in the placebo group after a mean of 5.5 months of therapy were -3 +/- 3, -1 +/- 2, -8 +/- 4, and -18 +/- 5 percent, respectively; there was significant improvement in the lovastatin group, which had responses of 3 +/- 3, 3 +/- 3, 0 +/- 2, and 0 +/- 3 percent (P = 0.004). CONCLUSIONS: Cholesterol lowering with lovastatin significantly improved endothelium-mediated responses in the coronary arteries of patients with atherosclerosis. Such improvement in the local regulation of coronary arterial tone could potentially relieve ischemic symptoms and signal the stabilization of the atherosclerotic plaque.

Lack of effect of lovastatin on restenosis after coronary angioplasty. Lovastatin Restenosis Trial Study Group.

BACKGROUND: Experimental and clinical observations suggest that lowering serum lipid levels may reduce the risk of restenosis after coronary angioplasty. We report the results of a prospective, randomized, double-blind trial evaluating whether lowering lipid levels with lovastatin can prevent or delay restenosis after angioplasty. METHODS: Seven to 10 days before angioplasty, we randomly assigned eligible patients to receive lovastatin (40 mg orally twice daily) or placebo. Patients who underwent successful, complication-free, first-time angioplasty of a native vessel (the index lesion) continued to receive therapy for six months, when a second coronary angiogram was obtained. The primary end point was the extent of restenosis of the index lesion, as assessed by quantitative coronary arteriography. Of 404 patients randomly assigned to study groups, 384 underwent angioplasty; 354 of the procedures were successful, and 321 patients underwent angiographic restudy at six months. RESULTS: At base line, the patients in the lovastatin group (n = 203) and the placebo group (n = 201) were similar with respect to demographic clinical, angiographic, and laboratory characteristics. At base line the mean (+/- SD) degree of stenosis, expressed as a percentage of the diameter of the vessel, was 64 +/- 11 percent in the lovastatin group, as compared with 63 +/- 11 percent in the placebo group (P = 0.22). Despite a 42 percent reduction in the serum level of low-density lipoprotein cholesterol in the lovastatin group, after six months of treatment the amount of stenosis seen in the second angiogram was 46 +/- 20 percent in the placebo group, as compared with 44 +/- 21 percent in the lovastatin group (P = 0.50). Similarly, there were no significant differences in minimal luminal diameter or other measures of restenosis. A trend was noted toward more myocardial infarctions in the lovastatin group, as a result of acute vessel closure or restenosis at the site of angioplasty, but there were no other important differences between the two groups in the frequency of fatal or nonfatal events at six months. CONCLUSIONS: Treatment with high-dose lovastatin initiated before coronary angioplasty does not prevent or delay the process of restenosis in the first six months after the procedure.

Longitudinal force focused coronary angioplasty: a technique for resistant lesions.

In a small percentage of vascular lesions undergoing angioplasty, the force generated by balloon inflation is insufficient to produce an acceptable deformation of the stenosis. Techniques developed to deal with this problem include the use of laser energy and rotational atherectomy. Use of a guidewire positioned between the dilating balloon and vessel wall has been reported to be effective in resistant heavily calcified lesions. The current case report describes a situation in which two wires between the balloon and the target lesion were required to produce an acceptable reduction in stenosis severity. This technique represents an extension of the single-wire technique and may have relevance to the strategy being explored with the "cutting balloon."

Catastrophic thrombus development despite systemic heparinization during coronary angioplasty: possible relationship to nonionic contrast.

Two cases of catastrophic thrombus formation during coronary angioplasty occurred shortly after the operators began using nonionic contrast. This occurred despite systemic heparinization, the adequacy of which was documented by activated clotting times (ACT). Both cases were resistant to balloon inflation and one was refractory to intracoronary thrombolysis. There is a considerable body of evidence documenting that low-osmolality contrast media, especially those that are nonionic, have less anticoagulant effect than standard contrast media. Several reports have also been published suggesting possible relationships between nonionic contrast and intravascular thrombus formation during coronary angiography and angioplasty. These data are reviewed and recommendations made for utilization of these contrast media.

Fractured and retained guide-wire fragment during coronary angioplasty--unforeseen late sequelae.

During a difficult coronary angioplasty, the tip of the guide wire became inadvertently wedged in a distal vessel, fractured, and retained in situ. Because of the otherwise successful nature of the angioplasty and the patient's great risk for cardiac surgery, it was elected to leave the wire fragment in place. Recurrence of symptoms led to recatheterization, which in addition to restenosis of the original angioplasty site showed diffuse narrowing of the arterial segment that contained the retained wire fragment. This occurred despite systemic anticoagulation with Coumadin in the interval between procedures. Thus retained guide wire fragments in patent coronary arteries may cause arterial narrowing despite systemic anticoagulation.