Echocardiography in patients with hypertrophic cardiomyopathy: usefulness of old and new techniques in the diagnosis and pathophysiological assessment

Hypertrophic cardiomyopathy (HCM) is one of the most common inherited cardiomyopathy. The identification of patients with HCM is sometimes still a challenge. Moreover, the pathophysiology of the disease is complex because of left ventricular hyper-contractile state, diastolic dysfunction, ischemia and obstruction which can be coexistent in the same patient. In this review, we discuss the current and emerging echocardiographic methodology that can help physicians in the correct diagnostic and pathophysiological assessment of patients with HCM

Role of ultrasound in the non-invasive evaluation of coronary vasodilator capacity in systematic hypertension | [L'ecocardiografia nella valutazione non invasiva della riserva coronarica e della perfusione miocardica nell'ipertensione arteriosa]

Systemic hypertension is associated with structural and functional alterations of the coronary circulation, which increase the susceptibility of the hypertensive heart to myocardial ischemia. The spectrum of modifications in the coronary macro and microcirculation of the hypertensive heart is relatively wide, and their assessment requires advanced and possibly non-invasive diagnostic approaches. This paper describes the possibility and the additive value of myocardial contrast echocardiography and of coronary velocimetry by Doppler echocardiography for the assessment of coronary function in hypertensive subjects

Surrogate end points of antihypertensive treatment: Left ventricular hypertrophy and structural alteration of carotid arteries

The present paper provides a critical overview of left ventricular hypertrophy (LVH) and structural changes of carotid arteries as surrogate end points for antihypertensive treatments. LVH is known to be associated with a number of pathophysiologic alterations underlying cardiovascular risk. The quantification of left ventricular mass is feasible and well standardized by echocardiography, even if the reproducibility of measurements is still limited. LVH has been clearly demonstrated to be an independent predictor for cardiovascular morbidity and mortality, and recent data suggest that left ventricular geometric pattern and depressed myocardial function may represent additional risk factors. Although clinical trials have shown that an adequate blood pressure control can be associated with a significant reduction in left ventricular mass, the prognostic impact of LVH regression is still debated. Serial measurements of the carotid artery intima-media complex by B-mode ultrasound have been proposed as an accurate noninvasive approach for the evaluation of progression and regression of the atherosclerotic process over time. The methodology of measurement is not as well standardized as that of LVH, and the reproducibility of measurements is too close to the magnitude of structural changes over time. In addition, sounder data are required concerning the pathophysiologic relationship between carotid lesions and clinical events

Vasodilation to bradykinin is mediated by an ouabain-sensitive pathway as a compensatory mechanism for impaired NO availability in essential hypertensive patients

Background - In essential hypertension, endothelium-dependent vasodilation is impaired because of reduced nitric oxide (NO) availability, which is mainly caused by oxidative stress. The present study was designed to identify the mechanism(s) responsible for NO-independent vasodilation to bradykinin in patients with essential hypertension. Methods and Results - In 16 healthy subjects (49.5±5.8 years; 118.6±3.5/78.9±2.9 mm Hg) and 16 patients with essential hypertension (47.9±4.8 years; 154.6±4.5/102.9±3.2 mm Hg), we measured modifications in forearm blood flow (strain-gauge plethysmography) during intrabrachial infusion of bradykinin (5, 15, or 50 ng/100 mL of forearm tissue per minute) in the presence of saline, N(ω)- monomethyl-L-arginine (L-NMMA; used to inhibit NO synthase; 100 μg/100 mL of forearm tissue per minute), and ouabain (to block Na+K+/ATPase and prevent hyperpolarization; 0.7 μg/100 mL of forearm tissue per minute). In healthy subjects, vasodilatation to bradykinin was significantly blunted by L-NMMA and unaffected by ouabain. In hypertensive patients, vasodilatation to bradykinin was not modified by L-NMMA, but it was significantly reduced by ouabain. In an adjunctive group of 8 hypertensive patients (49.9±3.8 years; 155.9±5.5/103.7±3.9 mm Hg), the response to bradykinin was repeated during the administration of intrabrachial vitamin C (a scavenger for oxygen free radicals; 8 mg/100 mL of forearm tissue per minute). In these patients, L- NMMA-induced inhibition of vasodilation to bradykinin was restored, and ouabain was no longer effective. In a final group of 6 normotensive controls (45.9±4.1 years; 115.1±2.9/79.3±2.1 mm Hg), vasodilation to bradykinin residual to L-NMMA blockade was further inhibited by simultaneous ouabain infusion. Conclusions - Vasodilation to bradykinin is impaired in essential hypertensive patients because of an NO-system alteration caused by oxidative stress, and it is mediated by an alternative pathway, possibly involving endothelium-dependent hyperpolarization

Effect of acute blood pressure reduction on endothelial function in the brachial artery of patients with essential hypertension

OBJECTIVES: To evaluate the effect of acute blood pressure reduction on endothelium-dependent vasodilation in the peripheral circulation of essential hypertensive patients. DESIGN: A parallel group study; endothelial function measured in 64 essential hypertensive patients before and after (2 h) treatment with nifedipine (20 mg, n = 32) or captopril (50 mg, n = 32), p.o., randomly assigned. METHODS: In hypertensive patients, we evaluated flow-mediated, endothelium-dependent dilation (FMD, high resolution ultrasound) of the brachial artery compared with endothelium-independent response to glyceryl trinitrate (GTN, 25 microg s.l.). Automatic computerized analysis was used to measure brachial artery diameter on end-diastolic frames acquired every second during the study. Sixty-six healthy normotensive subjects were also evaluated to assess the presence of endothelial dysfunction in hypertensive patients. RESULTS: Hypertensive patients showed a significantly (P< 0.01) lower FMD (5.9 +/- 2.5%) as compared to healthy controls (7.7 +/- 3.8%). The response to GTN was similar in normotensive subjects (7.5 +/- 3.1%) and hypertensive patients (7.2 +/- 6.5%). At baseline brachial artery diameter, FMD and response to GTN were similar in the nifedipine- and captopril-treated groups. Nifedipine and captopril similarly reduced blood pressure, but only nifedipine increased heart rate. Acute nifedipine, but not captopril, significantly (P< 0.01) increased brachial artery diameter, while FMD and response to GTN were not modified after nifedipine or captopril. CONCLUSIONS: Endothelial dysfunction in the brachial artery of essential hypertensive patients is not improved by acute blood pressure reductio