[Regression of left ventricular hypertrophy in hypertensive heart disease]. / 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.

Diminished coronary reserve in patients with biopsy-proven inflammatory infiltrates.

OBJECTIVE: We tested the hypothesis that patients with biopsy-proven inflammatory infiltrates have an impaired vasodilator capacity of the coronary microvasculation. METHODS: In 80 patients with clinically suspected inflammatory heart disease, coronary regulation was assessed with the argon method (1) at rest and maximal coronary flow (V(cor)/V(max)) and (2) at rest and minimal coronary resistance (R(cor)/R(min)) both before and after dipyridamole (0.5 mg/kg body weight) treatment. RESULTS: Compared to patients without evidence of myocardial inflammation in endomyocardial biopsy (n = 51) but similar demographic characteristics, patients with biopsy-proven inflammatory infiltrates (n = 29) showed significantly reduced maximal coronary flow (286 +/- 122 vs. 189 +/- 78 ml/min x 100 g; p = 0.001) and minimal coronary resistance was increased (0.40 +/- 0.17 vs. 0.60 +/- 0.27 mm Hg x min x 100 g/ml(-1), p = 0.001). The coronary reserve in patients with inflammatory infiltrates was markedly reduced (3.5 +/- 1.1 to 2.4 +/- 0.81, p = 0.001). CONCLUSION: Patients with biopsy-proven inflammatory infiltrates have a diminished coronary reserve due to reduced coronary vasodilator capacity. This may be due to the involvement of the intramural coronary vasculature in inflammatory heart disease.

Elevated serum markers of collagen degradation in patients with mild to moderate dilated cardiomyopathy.

BACKGROUND AND AIMS: Left ventricular (LV) dilation and myocardial remodelling are hallmarks of heart failure in idiopathic dilated cardiomyopathy (DCM). Interstitial collagen is essential for LV integrity and function while degradation of collagen by collagenases, especially matrix-metalloproteinases (MMPs), are suggested to contribute to ventricular dilation. In the present study, serological markers of collagen metabolism were investigated. METHODS AND RESULTS: Serum levels of MMP-1 and its inhibitor (TIMP-1), the markers for collagen degradation type I (collagen carboxyterminal telopeptide (ICTP)) and synthesis (carboxyterminal propeptide of type I procollagen (PICP)) were quantified by ELISA and RIA of 43 patients with DCM and 47 age-matched control subjects. Free MMP-1 serum concentration was significantly increased in the DCM group (5.29+/-0.83 vs. 2.22+/-0.29 ng/ml; P=0.01) as well as the free TIMP-1 concentration (206.54+/-12.65 vs. 181.44+/-8.55 ng/ml; P=0.05). The free MMP-1/TIMP-1-ratio was higher in DCM than in the control group (0.030+/-0.005 vs. 0.012+/-0.001; P=0.01). ICTP was significantly increased (7.60+/-1.21 vs. 3.44+/-0.19 microg/l; P<0.001). PICP was not significantly increased (125.29+/-8.93 microg/l vs. 113.11+/-5.47 microg/l; P=n.s.). Free MMP-1 and MMP-1/TIMP-1-ratio correlated with LV end diastolic diameter [cm/m(2) body surface area (BSA)] (r=0.28; P=0.03 and r=0.34; P=0.01, respectively) as well as with cardiac index (CI) (r=-0.32; P=0.04 and r=-0.33; P=0.04, respectively) in patients with DCM. CONCLUSION: Serum markers of collagen degradation are elevated and might be valuable markers for progression of LV dilation in patients with DCM.