Transoesophageal echocardiographic evaluation of right and left pulmonary arteries, up to the origin of their lobar branches, was prospectively performed with a single plane probe in 32 consecutive patients (18M, 14F, aged 55.5 ± 14.6, from 32 to 80 years) with clinical or echocardiographic suspicion of pulmonary embolism, who met transthoracic echocardiographic criteria of right ventricular overload Transoesophageal echocardiography showed unequivocal (20 patients) or suspected (three patients) intraluminar thrombi in 88.5% of 26 patients with haemodynamically significant acute or chronic pulmonary embolism, confirmed with reference methods. The sensitivity of the unequivocal transoesophageal echocardiographic diagnosis was 80% for acute and 73% for chronic haemodynamically significant pulmonary embolism. No false-positive results were found (specificity 100%). Additionally, in three cases, transoesophageal echocardiography disclosed the cause of the right ventricular overload revealing a previously undiagnosed atrial septal defect or Ebstein anomaly. Direct visualization of proximal pulmonary arterial thrombi by transoesophageal echocardiography emerges as a useful new method of prompt and definite diagnosis of haemodynamically important pulmonary embolism.

Primary aldosteronism (PA) is a potentially curable form of secondary hypertension caused by excessive renin-independent aldosterone secretion, leading to increased target organ damage and cardiovascular morbidity and mortality. The diagnosis of PA requires measuring renin and aldosterone to calculate the aldosterone-to-renin ratio, followed by confirmatory tests to demonstrate renin-independent aldosterone secretion and/or PA subtype differentiation. Various antihypertensive drug classes interfere with the renin-angiotensin-aldosterone axis and hence evaluation for PA should ideally be performed off-drugs. This is, however, often precluded by the risks related to suboptimal control of blood pressure and serum potassium level in the evaluation period. In the present review, we summarized the evidence regarding the effect of various antihypertensive drug classes on biochemical testing for PA, and critically appraised the issue whether and which antihypertensive medications should be withdrawn or, conversely, might be continued in patients evaluated for PA. The least interfering drugs are calcium antagonists, alpha-blockers, hydralazine, and possibly moxonidine. If necessary, the testing may also be attempted during treatment with beta-blockers, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers but renin and aldosterone measurements must be interpreted in the context of known effects of these drugs on these parameters. Views are evolving on the feasibility of testing during treatment with mineralocorticoid receptor antagonists, as these drugs are now increasingly considered acceptable in specific patient subsets, particularly in those with severe hypokalemia and/or poor blood pressure control on alternative treatment.

Neuropeptide-Y (NPY) is a peptide proposed to modulate the effect of the sympathetic nervous system on blood pressure control and contribute to the development of essential hypertension. To assess the possible influence of gender on its role, we evaluated plasma NPY, noradrenaline (NA) and adrenaline (A) concentrations in men and women with essential hypertension. No difference in NPY concentration was found between genders, but NPY concentration was elevated in both hypertensive men and women. NA levels were similar in all investigated hyper- and normotensives, while A was increased only in hypertensive men. These results suggest various patterns of sympatho-adrenal activity in gender subgroups of patients with essential hypertension.

Estimated 24-hour urinary creatinine excretion (24 hrUCr) may be useful for converting spot urine analyte/creatinine ratio into estimated 24-hour urinary excretion of the evaluated analyte, and for verifying completeness of 24-hour urinary collections. We compared various published 24 hrUCr-estimating equations against measured 24 hrUCr in hospitalized hypertensive patients. 24 hrUCr was measured in 293 patients and estimated using eight formulas (CKD-EPI, Cockcroft-Gault, Walser, Goldwasser, Rule, Gerber-Mann, Kawasaki, Tanaka). We used the Pearson correlation coefficient, the Bland-Altman method, and the percentage of estimated 24 hrUCr within 15%, 30% (P30), and 50% of measured 24hUCr to compare estimated and measured 24 hrUCr. Differences between the mean bias by eight formulas were evaluated using the Friedman rank sum test. Overall, the best formulas were CKD-EPI (mean bias 0.002 g/d, P30 86%) and Rule (mean bias 0.022 g/d, P30 89%), although both tended to underestimate 24 hrUCr with higher excretion values. The Gerber-Mann formula and the Asian formulas (Tanaka, Kawasaki) were less precise in our study population but superior in an analysis restricted to subjects with highest measured 24 hrUCr per body weight. We found significant differences between 24 hrUCr-estimating equations in hypertensive patients. In addition, formula performance was critically affected by inclusion criteria based on measured 24 hrUCr per body weight.

Owing to inconvenience of a 24‑hour urine collection, diagnostic methods based on spot urine samples are becoming increasingly popular. Spot urine sodium measurements could replace 24‑hour urinary sodium (24hUNa) excretion, considered a surrogate measure of dietary sodium intake. Spot urine-based approaches to estimating 24hUNa and 24‑hour urinary potassium (24hUK) excretion are potentially useful in patients with hypertension, for example, to identify increased urinary potassium excretion in individuals with primary aldosteronism and high dietary sodium intake in those with resistant hypertension. In this review, we summarized our research on spot urine-based estimation of 24hUNa, 24hUK, and 24‑hour urinary creatinine (24hUCr) excretion to avoid the need for a 24‑hour urine collection in patients with hypertension. We found that the Pan American Health Organization (PAHO) formula was generally the best for predicting the average 24hUNa and 24hUK excretion in hospitalized patients with hypertension, while the Kawasaki equation was inferior for estimating 24hUNa and the Tanaka equation was inferior for estimating 24hUK excretion. However, all 3 equations were imprecise in terms of estimating individual 24hUNa or 24hUK excretion. We also confirmed the general utility of the equations for estimating 24hUCr excretion in hypertensive individuals but with significant differences between various equations, the best formulas being Chronic Kidney Disease Epidemiology Collaboration (CKDEPI) and Rule. Compared with the combined PAHO/CKD‑EPI formula, the Tanaka and Kawasaki equations underestimated increased 24hUNa and 24hUK excretion. Thus, the combined PAHO/CKD‑EPI formula might be the best for identifying increased 24hUNa and 24hUK excretion in patients with hypertension.