Beta-oxidation of 1-[14C]-17-[131I]-iodoheptadecanoic acid following intracoronary injection in humans results in similar release of both tracers

Radioiodine labelled 17-iodo-heptadecanoic acid (IHA) is used for non-invasive study of myocardial metabolism in coronary heart disease and cardiomyopathy. Yet in the interpretation of in vivo myocardial tracer kinetics, it is controversial whether the intracellular degradation of IHA or the removal of iodide across cellular membranes is the rate-limiting step in iodide release from the myocardium. In five patients undergoing coronary sinus catheterization, a mixture of about 40 kBq of [¹²³I] NaI was injected into the left coronary artery. During the following 15-min period, frequent blood samples were taken from the aorta and the coronary sinus. In the aqueous phase of the venous blood, ¹⁴CO₂ and inorganic ¹³¹I appeared nearly in parallel, with a peak time of 4–5 min. Moreover, as shown by the AV difference, there was no significant back diffusion of IHA and no significant non-specific deiodination detectable over the period of observation. There was myocardial retention of inorganic iodide (¹²³I) injected into the left coronary artery. The data strongly support the premise that lipid turnover through -oxidation is the rate-limiting step in the externally measured release of iodide after IHA injection, provided that recirculating inorganic radioactive iodide is corrected for. In addition, 15 volunteers were studied using [¹¹C]palmitic acid and [¹²³I]IHA using PET and dynamic planar camera scintigraphy with iodide correction. There was no significant difference between the mean values of the elimination half-times, and also no significant correlation between half-times of both fatty acids for single individuals.     

Evaluation of myocardial function with the 201thallium scintimetry in various diseases of the heart. A correlative study based on 100 patients.

To assess the validity of the quantitative 201Tl scintimetry in various diseases of the heart (coronary heart disease with and without myocardial infarction, non-coronary cardiomyopathy, scleroderma heart disease and asymmetric septal hypertrophy with IHSS), the 201Tl myocardial uptake values for five standardized projections (a) were correlated with the grade of LAD stenosis, (b) the pattern of myocardial wall motion and (c) were compared with the 201Tl uptake values derived from normal patients. Significant reduction (c) of 201Tl myocardial uptake could in individual cases be evaluated in acute myocardial infarction (95%), in dys- and akinesia (90%), in hypokinesia (71%), in scleroderma heart disease (50%), in non-coronary cardiomyopathy (50%) as well as in normokinesia (28%) when associated with LAD stenosis. The mean values (b) of 201Tl uptake in normo- and hypokinesia significantly differed between these two groups and from those evaluated in dys- and akinesia. The latter group showed the lowest 201Tl uptake values computed which in some cases were very close to the mean mediastinal 201Tl uptake. The correlation (a) of individual 201Tl values demonstrated that 201Tl distribution in the myocardium is not only equivalent to myocardial "perfusion' but is corresponding with the myocardial function. In non-coronary cardiomyopathy reduced 201Tl values sometimes could not be separated from values in coronary heart disease (and myocardial infarction). A regional increase of myocardial mass as in septal hypertrophy correlated well with an augmented 201Tl uptake when referred to the 201Tl storage in the mediastinum.     

Intracoronary administration of dipyridamole prior to percutaneous transluminal coronary angioplasty provides a protective effect exceeding that of ischemic preconditioning

BACKGROUND: Ischemic preconditioning renders hearts more resistant to the deleterious consequences of ischemia. Adenosine is an important mediator in the induction and maintenance of ischemic preconditioning. Percutaneous transluminal coronary angioplasty (PTCA) allows the investigation of the consequences of ischemia in humans. The severity of myocardial ischemia decreases with subsequent balloon inflations during the course of PTCA. OBJECTIVE: To compare the effect of intracoronary administration of dipyridamole with the effect of consecutive balloon inflations. METHODS: We investigated 30 patients undergoing PTCA of the left anterior descending coronary artery in the setting of stable angina pectoris. Patients were randomly allocated to be administered either 0.5 mg/kg body weight dipyridamole intracoronarily or an equal amount of saline. Patients administered saline served as a control group. All patients were subjected to three consecutive balloon inflations. Severity of myocardial ischemia was assessed in terms of severity of chest pain, electrocardiographic signs of ischemia, and duration of balloon inflation tolerated. RESULTS: Patients administered dipyridamole intracoronarily tolerated significantly longer durations of balloon inflation than did patients in the control group. Severity of anginal pain and extent of electrocardiographic signs of ischemia were significantly lower after intracoronary administration of dipyridamole. The reductions in anginal pain and ST-segment shift caused by intracoronary administration of dipyridamole during the first balloon inflation were even more pronounced than the protection that was afforded by the third balloon inflation for patients in the control group. CONCLUSIONS: Intracoronary administration of dipyridamole prior to PTCA is associated with a significant gain in tolerance of ischemia. The protection afforded by intracoronary administration of dipyridamole is even more pronounced than the effect of ischemic preconditioning.     

Restenosis after elective coronary balloon angioplasty in patients with end stage renal disease: a case-control study using quantitative coronary angiography

Objective—To assess the rate of angiographic restenosis in patients with end stage renal disease after elective coronary angioplasty.
Design—A retrospective case-control study of 20 patients with end stage renal disease and 20 sex and age matched controls without renal disease, who had undergone primarily successful coronary angioplasty. Control coronary angiography was performed regardless of worsening or renewed incidence of anginal symptoms.
Main outcome measures—Group comparison of coronary morphology, as evaluated by quantitative coronary angiography, and of cardiovascular risk factors.
Results—The rate of angiographic restenosis was 60% in patients with renal disease and 35% in controls. In patients with end stage renal disease the following differences (mean (SD) were found versus controls: raised plasma fibrinogen (483 (101) v 326 (62) mg/dl, p < 0.001); raised plasma triglyceride (269 (163) v 207 (176) mg/dl, p < 0.01); smaller diameter of the coronary reference segment (2.59 (0.87) v 2.90 (0.55) mm, p < 0.10); smaller minimum luminal diameter of the dilated stenosis (0.77 (0.46) v 0.97 (0.27) mm, p < 0.05). Discriminant analysis showed that minimum luminal diameter before angioplasty (r = −0.79) and fibrinogen (r = +0.34) had the highest statistical association with restenosis.
Conclusions—The high rate of angiographic restenosis in patients with end stage renal disease seems to be related to the size of the vessel dilated and to an increased prothrombotic risk, as indicated by higher fibrinogen concentrations.

Keywords: renal disease;  coronary artery disease;  coronary angioplasty;  restenosis     

Hypertrophieregression als Therapieprinzip des Hochdruckherzens

PATHOPHYSIOLOGY AND THERAPY: Left ventricular hypertrophy represents an important factor determining the prognosis of hypertensive patients. Hypertrophy as identified by electrocardiography (Table 1) or echocardiography (Table 2) characterizes patients with a significantly increased risk of mortality and arrhythmia. From the pathophysiological point of view this is based on hypertrophy of the media in resistance vessels, on interstitial fibrosis, on a reduced coronary flow reserve and on the occurrence of ischemia (Figure 1). The diastolic and (later) systolic function of the heart are disturbed (Figures 2 to 4). Antihypertensive therapy with beta blockers and diuretics leads to a reduction of left ventricular mass by 5-8%, with ACE-inhibitors and AT-blockers by 13% (Figure 5). Particularly ACE-inhibitors can effectively reverse of the above mentioned pathological processes. Regression of hypertrophy goes along with an improved prognosis and a reduction of atrial and ventricular arrhythmias (Figure 6). A symptomatic treatment of arrhythmias should always be accompanied by medical therapy aimed at regression of hypertrophy. Optimal therapy results in normalizes of blood pressure, leads to a regression of hypertrophy and induces cardiac reparation, which in turn improve left ventricular function, reduces microvascular ischemia stress and arrhythmias. These therapeutic desiderates are also pertinent for hypertensive heart disease in the prehypertrophic state, as in juvenile hypertension.