Jerzy Gąsowski

Prof. Dr. Jerzy Gąsowski

Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, 2 Jakubowskiego St., 30-668 Krakow, Poland

Research Focus & Metrics

Academic Career Length

29Years (1998-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 March 2000 in The Lancet
Verified
Journal Article
Closed access
JSJan Albert Staessen
Jan Albert Staessen
Jerzy GąsowskiJerzy Gąsowski
Jerzy Gąsowski
JWJi G Wang
Ji G Wang
LTLutgarde Thijs
Lutgarde Thijs
EHElly Den Hond
Elly Den Hond
RFRobert H Fagard
Robert H Fagard

24 April 2000 in Archives of internal medicine (1960)
Verified
Journal Article
Open access
PDF file
JBJacques Blacher
Jacques Blacher
JSJan Albert Staessen
Jan Albert Staessen
XGXavier Girerd
Xavier Girerd
Jerzy GąsowskiJerzy Gąsowski
Jerzy Gąsowski
LTLutgarde Thijs
Lutgarde Thijs
MSMichel E. Safar
Michel E. Safar
ARTERIAL HYPERTENSION mechanically stresses the endothelium and the deeper layers of the arterial wall. The ensuing arterial lesions lead in the long run to debilitating and lethal complications, in particular stroke and myocardial infarction. The current guidelines for the management of hypertension rest almost completely on the measurement of systolic and diastolic blood pressure, 2 specific inflection points of the blood pressure wave, which are usually considered in isolation.1,2 However, blood pressure propagates through the arterial tree as a repetitive continuous wave and is more accurately described as consisting of a pulsatile component (pulse pressure) and a steady component (mean pressure).3 The former depends on ventricular ejection, arterial stiffness, and the timing of wave reflections, whereas cardiac output and peripheral vascular resistance are the major determinants of mean pressure.

5 September 2000 in Circulation
Verified
Journal Article
Closed access
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RFRobert H. Fagard
Robert H. Fagard
JSJan Albert Staessen
Jan Albert Staessen
LTLutgarde Thijs
Lutgarde Thijs
Jerzy GąsowskiJerzy Gąsowski
Jerzy Gąsowski
CBChristopher J. Bulpitt
Christopher J. Bulpitt
JWJohn Webster
John Webster
Background —The goal of the present study was to assess the effect of antihypertensive therapy on clinic (CBP) and ambulatory (ABP) blood pressures, on ECG voltages, and on the incidence of stroke and cardiovascular events in older patients with sustained and nonsustained systolic hypertension. Methods and Results —Patients who were ≥60 years old, with systolic CBP of 160 to 219 mm Hg and diastolic CBP of <95 mm Hg, were randomized into the double-blind placebo-controlled Systolic Hypertension in Europe (Syst-Eur) Trial. Treatment consisted of nitrendipine, with the possible addition of enalapril, hydrochlorothiazide, or both. Patients enrolled in the Ambulatory Blood Pressure Monitoring Side Project were classified according to daytime systolic ABP into 1 of 3 subgroups: nonsustained hypertension (<140 mm Hg), mild sustained hypertension (140 to 159 mm Hg), and moderate sustained hypertension (≥160 mm Hg). At baseline, patients with nonsustained hypertension had smaller ECG voltages ( P <0.001) and, during follow-up, a lower incidence of stroke ( P <0.05) and of cardiovascular complications ( P =0.01) than other groups. Active treatment reduced ABP and CBP in patients with sustained hypertension but only CBP in patients with nonsustained hypertension ( P <0.001). The influence of active treatment on ECG voltages ( P <0.05) and on the incidence of stroke ( P <0.05) and cardiovascular events ( P =0.06) was more favorable than that of placebo only in patients with moderate sustained hypertension. Conclusions —Patients with sustained hypertension had higher ECG voltages and rates of cardiovascular complications than did patients with nonsustained hypertension. The favorable effects of active treatment on these outcomes were only statistically significant in patients with moderate sustained hypertension.

30 July 2021 in Aging Clinical and Experimental Research
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KPKarolina Piotrowicz
Karolina Piotrowicz
Jerzy GąsowskiJerzy Gąsowski
Jerzy Gąsowski
JMJean-Pierre Michel
Jean-Pierre Michel
NVNicola Veronese
Nicola Veronese
In this review, we discuss the pathophysiologic and management aspects of acute sarcopenia in relation to SARS-CoV-2 infection. COVID-19 is as a multi-organ infectious disease characterized by a severe inflammatory and highly catabolic status, influencing the deep changes in the body build, especially the amount, structure, and function of skeletal muscles which would amount to acutely developed sarcopenia. Acute sarcopenia may largely impact patients’ in-hospital prognosis as well as the vulnerability to the post-COVID-19 functional and physical deterioration. The individual outcome of the COVID-19 and the degree of muscle mass and functional loss may be influenced by multiple factors, including the patient’s general pre-infection medical and functional condition, especially in older adults. This paper gathers the information about how the SARS-CoV-2 hyper-inflammatory involvement exacerbates the immunosenescence process, enhances the endothelial damage, and due to mitochondrial dysfunction and autophagy, induces myofibrillar breakdown and muscle degradation. The aftermath of these acute and complex immunological SARS-CoV-2-related phenomena, augmented by anosmia, ageusia and altered microbiota may lead to decreased food intake and exacerbated catabolism. Moreover, the imposed physical inactivity, lock-down, quarantine or acute hospitalization with bedrest would intensify the acute sarcopenia process. All these deleterious mechanisms must be swiftly put to a check by a multidisciplinary approach including nutritional support, early physical as well cardio-pulmonary rehabilitation, and psychological support and cognitive training. The proposed holistic and early management of COVID-19 patients appears essential to minimize the disastrous functional outcomes of this disease and allow avoiding the long COVID-19 syndrome.

1 January 2002 in Journal Of Hypertension
Verified
Journal Article
Closed access
Jerzy GąsowskiJerzy Gąsowski
Jerzy Gąsowski
RFRobert H. Fagard
Robert H. Fagard
JSJan Albert Staessen
Jan Albert Staessen
TGTomasz Grodzicki
Tomasz Grodzicki
SPStuart Pocock
Stuart Pocock
JBJean-Pierre Boissel
Jean-Pierre Boissel
Although current guidelines rest exclusively on the measurement of systolic and diastolic blood pressures, the arterial pressure wave is more precisely described as consisting of a pulsatile (pulse pressure) and a steady (mean pressure) component. This study explored the independent roles of pulse pressure and mean pressure as predictors of mortality in a wide range of patients with hypertension. This meta-analysis, based on individual patient data, has combined results from the control groups of seven randomized clinical trials conducted in patients with systolo-diastolic or isolated systolic hypertension. The relative hazard rates associated with pulse pressure and mean pressure were calculated using Cox's proportional hazard regression models with stratification for the seven trials and with adjustment for sex, age, smoking and the other pressure. A 10 mmHg wider pulse pressure at baseline, which corresponds to approximately one-half of its standard deviation, was independently associated with an increase in risk by 6% for total mortality (P = 0.001), 7% for cardiovascular mortality (P = 0.01), and 7% for fatal coronary accidents (P = 0.03).The corresponding increase in risk of fatal stroke was similar (+6%, P = 0.27) but there were too few strokes to reach statistical significance. In similar analyses, mean pressure was not identified as an independent predictor of these outcomes. Significant interactions of pulse pressure or mean pressure with age suggested that the prognostic power of pulse pressure for fatal stroke was more important at higher age (P = 0.04), whereas the prognostic power of mean pressure for coronary mortality was greatest in the young (P = 0.01). In hypertensive patients pulse pressure, not mean pressure, is associated with an increased risk of fatal events. This appears to be true in a broad range of patients with hypertension.

1 August 2001 in Journal of Human Hypertension
Verified
Journal Article
Closed access
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JSJan Albert Staessen
Jan Albert Staessen
JHJj van der Heijden-Spek
Jj van der Heijden-Spek
MSMe Safar
Me Safar
EHE Den Hond
E Den Hond
Jerzy GąsowskiJerzy Gąsowski
Jerzy Gąsowski
LBLm Van Bortel
Lm Van Bortel