Search

Your search keyword '"Moruzzi, P"' showing total 14 results
Start Over Author "Moruzzi, P" Topic hypertension
14 results on '"Moruzzi, P"'

2. Treatment of hypertension with calcium antagonists. Review.

Author

Guazzi MD, Polese A, Fiorentini C, Bartorelli A, and Moruzzi P

Subjects
Adrenal Gland Neoplasms complications, Antihypertensive Agents administration & dosage, Cardiomegaly drug therapy, Drug Therapy, Combination, Heart Failure drug therapy, Hemodynamics drug effects, Humans, Male, Methyldopa administration & dosage, Pheochromocytoma complications, Calcium Channel Blockers administration & dosage, Hypertension drug therapy, Nifedipine administration & dosage, Pyridines administration & dosage, Verapamil administration & dosage
Abstract

Calcium channel blockers have a selective action on the cardiovascular system. They reduce the energy requirement of the heart, reduce vascular smooth muscle tone, and increase systemic blood flow. Vasodilatation occurs in both the systemic and the pulmonary systems to an extent proportional to the baseline level of vascular resistance, and results in reduction of blood pressure when it is elevated. Thus, these blockers are useful in patients with high blood pressure. Clinical experience of calcium channel blockers in hypertension is so far confined almost exclusively to verapamil and nifedipine. This article reviews the advantages and limitations of these two compounds, their acute hemodynamic effects in hypertensive subjects, and their use in the treatment of hypertensive emergencies, hypertensive encephalopathy, and pheochromocytoma, and as ventricular afterload reducing agents in hypertensive left ventricular failure. Similarities in the effects of nifedipine on systemic and pulmonary vascular tone are presented as evidence that altered intracellular Ca++ concentration is involved in the vasoconstriction seen in both systems in systemic high blood pressure. They also provide support for the hypothesis that inappropriate Ca++ handling may be involved in maintaining elevated blood pressure in human hypertension.

Published
1983
Full Text
View/download PDF

4. Haemodynamic effects of a calcium antagonistic agent (nifedipine) in hypertension: therapeutic implications.

Author

Bartorelli C, Magrini F, Moruzzi P, Olivari MT, Polese A, Fiorentini C, and Guazzi M

Subjects
Humans, Hypertension physiopathology, Middle Aged, Nifedipine adverse effects, Nifedipine pharmacology, Hemodynamics drug effects, Hypertension drug therapy, Nifedipine therapeutic use, Pyridines therapeutic use
Abstract

1. In 27 severe primary hypertensive patients nifedipine (10 mg), administered orally, induced prompt (-21% of control at 30 min) and persistent (-17% at 120 min) fall of mean arterial pressure mediated through reduction of peripheral vascular resistance with rise of cardiac output. 2. The sublingual route (nine cases) showed more rapid onset of action and equal antihypertensive effectiveness. 3. In five patients with hypertensive crisis and acute left ventricular failure, the drug strikingly reduced systemic and pulmonary arterial pressures and relieved pulmonary oedema. 4. Prompt efficacy, ease of administration, absence of important side effects indicate that nifedipine may be a useful therapeutic agent in severe hypertension and in critical conditions that require rapid lowering of blood pressure.

Published
1978
Full Text
View/download PDF

5. The lesser circulation in patients with systemic hypertension.

Author

Guazzi MD, De Cesare N, Fiorentini C, Galli C, Moruzzi P, and Tamborini G

Subjects
Adult, Aorta physiopathology, Blood Pressure, Cold Temperature, Humans, Mathematics, Middle Aged, Pulmonary Circulation, Vascular Resistance, Blood Circulation, Hypertension physiopathology
Abstract

The elevated blood pressure and vascular resistance in patients with systemic hypertension are paralleled by a proportional rise in pressure and resistance in the lesser circulation. We evaluated the hypothesis that the increased systemic reaction to adrenergic stimulation is shared by the pulmonary vessels. For this purpose we investigated nine normotensive subjects and 24 patients with moderate primary hypertension during mental arithmetic and the cold pressor test. Both groups responded to both stimuli, with a pressure reaction that during arithmetic was mediated through an increase of cardiac output, and a reaction during the cold pressor test mediated through a predominant rise in systemic vascular resistance. The pressure changes were emphasized in the hypertensive population. Pressure in the pulmonary artery in normotensive subjects was not affected by cold and was slightly raised (systolic) during arithmetic. In hypertensive patients, on the other hand, systolic and diastolic pressures were consistently augmented by both tests, and pulmonary arteriolar resistance rose by 42% and 29% of control during the cold pressor test and arithmetic, respectively. Changes in resistance reflected neurally mediated vasoconstriction and not variations in the passive relationship between pressure and flow, since during arithmetic, for a similar rise in flow the driving pressure across the lungs was steady in normotensive subjects and rose significantly in hypertensive patients. In these same patients pressure was augmented by cold in the absence of substantial changes in flow. At baseline and during tests pulmonary wedge pressure, pleural pressure, arterial blood gases, and pH were similar in the two populations.(ABSTRACT TRUNCATED AT 250 WORDS)

Published
1987

6. Treatment of hypertension with nifedipine, a calcium antagonistic agent.

Author

Olivari MT, Bartorelli C, Polese A, Fiorentini C, Moruzzi P, and Guazzi MD

Subjects
Administration, Oral, Blood Pressure drug effects, Chemical Phenomena, Chemistry, Clinical Trials as Topic, Diastole, Drug Evaluation, Heart Rate drug effects, Humans, Male, Middle Aged, Monitoring, Physiologic, Nifedipine administration & dosage, Nifedipine adverse effects, Placebos, Pulmonary Circulation drug effects, Stroke Volume drug effects, Systole, Vascular Resistance drug effects, Calcium antagonists & inhibitors, Hypertension drug therapy, Nifedipine therapeutic use, Pyridines therapeutic use
Abstract

Hemodynamic monitoring after a single dose (10 mg) of nifedipine in 27 primary hypertensive subjects (diastolic pressure greater than 110 mm Hg) documented that this calcium antagonistic agent exerts a potent arteriolar vasodilating action, which results in prompt (-21% of control at 30 minutes) and persistent (-16% of control at 120 minutes) fall in mean arterial pressure associated with a rise in cardiac output and pulse rate. The same patients received oral treatment for 3 weeks. Hourly pressure readings showed that 1) the antihypertensive response to each dose lasts 8--12 hours; and 2) nifedipine every 6 hours significantly reduced blood pressure throughout the 24 hours, without postural hypotension. Side effect were short-lasting (headache in five patients, palpitation without arrhythmias in eight patients, burning sensation in the face and legs in five patients and sporadic extrasystoles in five patients) and tended to disappear with continued treatment. Development of drug resistance, sodium retention, plasma volume expansion, renin release or angina pectoris were not observed during the study. Although these findings seem to differentiate nifedipine from other vasodilators currently used in the treatment of hypertension, broader experience and more prolonged trials with nifedipine as an antihypertensive agent will be needed before conclusions can be drawn on these particular aspects.

Published
1979
Full Text
View/download PDF

7. Calcium channel blockade with nifedipine reduces the systemic and the pulmonary vascular reactivity to adrenergic activation in hypertension.

Author

Guazzi MD, Bartorelli A, Loaldi A, Moruzzi P, and Fiorentini C

Subjects
Adult, Humans, Hypertension drug therapy, Male, Calcium Channel Blockers therapeutic use, Epinephrine antagonists & inhibitors, Hypertension physiopathology, Nifedipine therapeutic use, Norepinephrine antagonists & inhibitors, Pulmonary Circulation drug effects, Vasomotor System drug effects
Abstract

In hypertension the systemic and the pulmonary circulation show exaggerated vascular tone and responsiveness to adrenergic stimuli. In 22 hypertensive men we tested whether the regulation of the two vascular beds is improved by calcium entry blockade with nifedipine. Mental arithmetic raised epinephrine plasma concentration (by 80%), cardiac output (CO) and blood pressure in both circuits, and caused systemic vasodilatation and pulmonary vasoconstriction. After the drug the epinephrine reaction was diminished (+20%), variations in CO and systemic blood pressure were almost unchanged and pulmonary vasoconstriction was abolished. A cold pressor test increased norepinephrine plasma concentration (by 24%), systemic and pulmonary pressure and resistance and did not alter CO. The norepinephrine response to cold was enhanced (+35%) by nifedipine, while systemic and pulmonary resistance rises were importantly attenuated (from +24% to +7% and from +41% to +1%, respectively), and greatly diminished the pressure reactivity. A sympatho-adrenal modulation by calcium blockade, per se, might have restrained the vasomotion during arithmetic. The impressive attenuation of the constrictor responses to cold, which was possibly associated with a potentiated sympathetic drive, prospects that the two circuits share a vascular contractile disorder in which calcium ions are involved.

Published
1986

10. Pulmonary vasoconstrictor overreactivity in borderline systemic hypertension.

Author

Moruzzi P, Sganzerla P, and Guazzi MD

Subjects
Adult, Cardiac Output, Catecholamines blood, Catheterization, Catheterization, Central Venous, Cold Temperature, Humans, Hypertension blood, Male, Stress, Psychological physiopathology, Vascular Resistance, Vena Cava, Inferior, Hypertension physiopathology, Pulmonary Circulation, Vasoconstriction
Abstract

Raised vascular pressure and resistance and vasoconstrictor overreactivity to adrenergic stimulation are hallmarks of the pulmonary circulation in sustained primary hypertension. The aim of this study was to investigate the reasons for these disorders. In 10 males with borderline systemic hypertension, pulmonary haemodynamic variables were similar to those of an age matched group of eight normotensive subjects. In normotension, arithmetic and cold pressor tests (sympathetic activators) caused slight vasodilatation and vasoconstriction, respectively. In hypertension both tests showed an obvious vasoconstrictor effect. Restriction of blood flow through the lungs by distension of a balloon in the inferior vena cava is known to increase pulmonary vasoconstrictor reactivity in normal man. As a result of this manoeuvre, pulmonary pressure fell in the normotensive controls without variation in pulmonary vascular resistance, whereas in the hypertensive group there was an increase in resistance and the pressure did not change. In normotensive subjects with caval balloon, the sympathetic activating stimuli both became constrictor and caused vascular resistance to rise to the levels attained in the hypertensive patients during adrenergic stimulation in the absence of obstruction to venous return. In the hypertensives, these stimuli were not able to enhance the pulmonary vascular resistance further. This shows that in these patients maximal vasoconstriction was already achieved through the simple restraint of blood flow with vena caval obstruction. We suggest that in the early phases of systemic hypertension lung vessels are hypercontractile so that they overreact to hypoperfusion or to sympathetic stimulation, even before there is a stable rise in pressure and resistance.

Published
1989
Full Text
View/download PDF

12. Combined hemodynamic overload of the left and right ventricles as a possible cause of interventricular septum preponderance in high blood pressure.

Author

Fiorentini C, Galli C, Tamborini G, Moruzzi P, Berti M, Riva S, and Guazzi MD

Subjects
Adult, Blood Pressure, Cardiac Output, Epinephrine blood, Female, Humans, Hypertension blood, Hypertension pathology, Male, Norepinephrine blood, Pulmonary Wedge Pressure, Stroke Volume, Heart Septum pathology, Hemodynamics, Hypertension physiopathology
Abstract

We tested whether overload of the two ventricles may be associated with a preponderance of interventricular septum in patients with high blood pressure. The rationale is that the septum is shared by the greater and lesser circulation and that in hypertension the latter shows the same qualitative hemodynamic alterations as the former. Among 65 hypertensive patients, 40 (group 1) showed (echo) posterior wall thickness within the mean +/- 1 SD of 62 normal subjects, and 25 (group 2) had a posterior wall thickness exceeding the mean + 1 SD of the normal population. Both groups were subdivided into subgroups A and B, which included patients whose ventricular septum was similar to (within the mean + 1 SD) and thicker than (exceeding the mean + 1 SD) the posterior wall thickness in the corresponding group, respectively. Resting differences in systemic and pulmonary pressure and vascular resistance among subgroups 1A, 1B, and 2A were not significant; however, in subgroup 2B these variables exceeded those in the other subgroups to a significant extent. During cold pressor testing (CPT) the levels reached and the changes in pressure and resistance from baseline values in both circuits were much greater in subgroups B than in subgroups A. The baseline plasma norepinephrine value showed a trend toward an increase from subgroup 1A to 1B and from subgroup 2A and 2B; during CPT norepinephrine invariably changed and in subgroups B it rose significantly more than in subgroups A. It was not determined whether this caused the hemodynamic overload in subgroups B.(ABSTRACT TRUNCATED AT 250 WORDS)

Published
1988
Full Text
View/download PDF

14. Atrial fibrillation management: A prospective survey in ESC Member Countries - The Euro Heart Survey on atrial fibrillation

Author

Nieuwlaat R., Capucci A., Camm A. J., Olsson S. B., Andresen D., Davies D. W., Cobbe S., Breithardt G., Le Heuzey J. -Y., Prins M. H., Levy S., Crijns H. J. G. M., Aliot E., Santini M., Vardas P., Manini M., Bramley C., Laforest V., Taylor C., Del Gaiso S., Huber K., De Backer G., Sirakova V., Cerbak R., Thayssen P., Lehto S., Blanc J. -J., Delahaye F., Kobulia B., Zeymer U., Cokkinos D., Karlocai K., Graham I., Shelley E., Behar S., Maggioni A., Grabauskiene V., Deckers J., Asmussen I., Stepinska J., Goncalves L., Mareev V., Vasiljevic Z., Riecansky I., Kenda M. F., Alonso A., Lopez-Sendon J. L., Rosengren A., Buser P., Okay T., Sychov O., Fox K., Schofield P., Simoons M., Wood D., Battler A., Boersma E., Komajda M., McGregor K., Mulder B., Priori S., Ryden L., Tavazzi L., Vahanian A., Wijns W., Grigoryan S. V., Apetyan I., Aroyan S., Azarapetyan L., Anvari A., Gottsauner-Wolf M., Pfaffenberger S., Aydinkoc K., Kalla K., Penka M., Drexel H., Langer P., Pierard L. A., Legrand V., Blommaert D., Schroeder E., Mancini I., Geelen P., Brugada P., De Zutter M., Vrints C., Vercammen M., Morissens M., Borisov B. B., Petrov V. A., Alexandrova M. M., Goudev A. R., Peychev Y., Stoyanovsky V., Stoynev E., Kranjcevic S., Moutiris J., Ioannides M., Evequoz D., Spacilova J., Novak M., Eisenberger M., Mullerova J., Kautzner J., Riedlbauchova L., Petru J., Taborsky M., Cappelen H., Sharaf Y. A., Ibrahim B. S. S., Tammam K., Saad A., Elghawaby H., Sherif H. Z., Farouk H., Mielke A., Engelen M., Kirchhof P., Zimmermann P., Aviles F. F., Rubio J., Malpartida F., Corona M., Sanchez L. T., Herrera J. M. L., Quesada A., Munoz Garcia A. J., Gonzalez C. S., Juango M. S. A., Berjon-Reyero J., Alegret J. M., Fernandez J. M. C., Rosillo C. C., Romero A. F., Lara M. G., Lopez Sendon J. L., De Diego J. J. G., Martin L. S., Irurita M., Guttierez N. H., Rubio J. R. S., Antorrena I., Paves A. B., Salvador A., Orriach M. D., Garcia A. A., Epelde F., Martinez V. B., Sanchez A. B., Galvez C. P., Rivero R. F., Madrid A. H., Baron-Esquivias G., Peinado R., Guindal J. A. G., Vera T. R., Fernandez E. L., Gayan R., Garcia J., Bodegas A., Lopez J. T., Florez J. M., Cabezas C. L., De Castroviejo E. V. R., Bellido J. M., Ruiz M. E., Savolainen K., Nieminen M., Toivonen L., Syvanne M., Pietila M., Galley D., Beltra C., Gay A., Daubert J. C., Lecocq G., Poulain C., Cleland J. G. F. C., Shelton R., Lip G. Y. H., Choudhury A., Abuladze G., Jashi I., Cokkinos D. V., Tsiavou A., Giamouzis G., Dagres N., Kostopoulou A., Domproglou Tsoutsanis, Stefanadis Ch., Latsios G., Vogiatzis I., Gotsis A., Bozia P., Karakiriou M., Koulouris S., Parissis J., Kostakis G., Kouris N., Kontogianni D., Athanasios K., Douras A., Tsanakis T., Marketou M., Patsourakos N., Czopf L., Halmosi R., Preda I., Csoti E., Badics A., Strasberg B., Freedberg N. A., Katz A., Zalzstein E., Grosbard A., Goldhammer E., Nahir M., Epstein M., Vider I., Luria D., Mandelzweig L., Aloisi B., Cavallaro A., Antonielli E., Doronzo B., Pancaldo D., Mazzola C., Buontempi L., Calvi V., Giuffrida G., Figlia A., Ippolito F., Gelmini G. -P., Gaibazzi N., Ziacchi V., De Tommasi F., Lombardi F., Fiorentini C., Terranova P., Maiolino P., Albunni M., Pinna-Pintor P., Fumagalli S., Masotti G., Boncinelli L., Rossi D., Santoro G. M., Fioranelli M., Naccarella F., Maranga S. S., Lepera G., Bresciani B., Seragnoli E., Forti M. C., Cortina V., Baciarello G., Cicconetti P., Lax A., Vitali F., Igidbashian D., Scarpino L., Terrazzino S., Cantu F., Pentimalli F., Novo S., Coppola G., Zingarini G., Ambrozio G., Moruzzi P., Callegari S., Saccomanno G., Russo P., Carbonieri E., Paino A., Zanetta M., Barducci E., Cemin R., Rauhe W., Pitscheider W., Meloni M., Marchi S. M., Di Gennaro M., Calcagno S., Squaratti P., Quartili F., Bertocchi P., De Martini M., Mantovani G., Komorovsky R., Desideri A., Celegon L., Tarantini L., Catania G., Lucci D., Bianchini F., Puodziukynas A., Kavoliuniene A., Barauskiene V., Aidietis A., Barysiene J., Vysniauskas V., Zukauskiene I., Kazakeviciene N., Georgievska-Ismail L., Poposka L., Vataman E., Grosu A. A., Scholte Op Reimer W., De Swart E., Lenzen M., Jansen C., Brons R., Tebbe H., Van Hoogenhuyze D. C. A., Veerhoek M. J., Kamps M., Haan D., Van Rijn N., Bootsma A., Baur L., Van Den Dool A., Fransen H., Eurlings L., Meeder J., De Boer M. J., Winter J., Broers H., Werter C., Bijl M., Versluis S., Milkowska M., Wozakowska-Kaplon B., Janion M., Lepska L., Swiatecka G., Kokowicz P., Cybulski J., Gorecki A., Szulc M., Rekosz J., Manczak R., Wnuk-Wojnar A. -M., Trusz-Gluza M., Rybicka-Musialik A., Myszor J., Szpajer M., Cymerman K., Sadowski J., Sniezek-Maciejewska M., Ciesla-Dul M., Gorkiewicz-Kot I., Grodzicki T., Rewiuk K., Kubik L., Lewit J., De Sousa J. M. F. R., Ferreira R., Freitas A., Morais J. C. A., Pires R., Veloso Gomes M. J., Gago P., Candeias R. A. C., Nunes L., Miranda Sa J. V., Ventura M., De Oliveira M., Alves L. B., Bostaca I., Olariu C. T., Dan G. A., Dan A., Podoleanu C., Frigy A., Georgescu G. I. M., Arsenescu C., Statescu C., Sascau R., Dimitrascu D. L., Rancea R., Shubik Y. V., Duplyakov D., Shalak M., Danielyan M., Galyavich A., Zakirova V., Hatala R., Kaliska G., Kmec J., Zupan I., Tasie J., Vokac D., Edvardsson N., Poci D., Gamra H., Denguir H., Sepetoglu A., Arat-Ozkan A., Orynchak M., Paliy E., Vakalyuk I., Malidze D., Prog R., Yabluchansky M. I., Makienko N. V., Potpara T., Knezevic S., Randjelovic M., Nieuwlaat R., Capucci A., Camm A.J., Olsson S.B., Andresen D., Davies D.W., Cobbe S., Breithardt G., Le Heuzey J.-Y., Prins M.H., Levy S., Crijns H.J.G.M., Aliot E., Santini M., Vardas P., Manini M., Bramley C., Laforest V., Taylor C., Del Gaiso S., Huber K., De Backer G., Sirakova V., Cerbak R., Thayssen P., Lehto S., Blanc J.-J., Delahaye F., Kobulia B., Zeymer U., Cokkinos D., Karlocai K., Graham I., Shelley E., Behar S., Maggioni A., Grabauskiene V., Deckers J., Asmussen I., Stepinska J., Goncalves L., Mareev V., Vasiljevic Z., Riecansky I., Kenda M.F., Alonso A., Lopez-Sendon J.L., Rosengren A., Buser P., Okay T., Sychov O., Fox K., Schofield P., Simoons M., Wood D., Battler A., Boersma E., Komajda M., McGregor K., Mulder B., Priori S., Ryden L., Tavazzi L., Vahanian A., Wijns W., Grigoryan S.V., Apetyan I., Aroyan S., Azarapetyan L., Anvari A., Gottsauner-Wolf M., Pfaffenberger S., Aydinkoc K., Kalla K., Penka M., Drexel H., Langer P., Pierard L.A., Legrand V., Blommaert D., Schroeder E., Mancini I., Geelen P., Brugada P., De Zutter M., Vrints C., Vercammen M., Morissens M., Borisov B.B., Petrov V.A., Alexandrova M.M., Goudev A.R., Peychev Y., Stoyanovsky V., Stoynev E., Kranjcevic S., Moutiris J., Ioannides M., Evequoz D., Spacilova J., Novak M., Eisenberger M., Mullerova J., Kautzner J., Riedlbauchova L., Petru J., Taborsky M., Cappelen H., Sharaf Y.A., Ibrahim B.S.S., Tammam K., Saad A., Elghawaby H., Sherif H.Z., Farouk H., Mielke A., Engelen M., Kirchhof P., Zimmermann P., Aviles F.F., Rubio J., Malpartida F., Corona M., Sanchez L.T., Herrera J.M.L., Quesada A., Munoz Garcia A.J., Gonzalez C.S., Juango M.S.A., Berjon-Reyero J., Alegret J.M., Fernandez J.M.C., Rosillo C.C., Romero A.F., Lara M.G., Lopez Sendon J.L., De Diego J.J.G., Martin L.S., Irurita M., Guttierez N.H., Rubio J.R.S., Antorrena I., Paves A.B., Salvador A., Orriach M.D., Garcia A.A., Epelde F., Martinez V.B., Sanchez A.B., Galvez C.P., Rivero R.F., Madrid A.H., Baron-Esquivias G., Peinado R., Guindal J.A.G., Vera T.R., Fernandez E.L., Gayan R., Garcia J., Bodegas A., Lopez J.T., Florez J.M., Cabezas C.L., De Castroviejo E.V.R., Bellido J.M., Ruiz M.E., Savolainen K., Nieminen M., Toivonen L., Syvanne M., Pietila M., Galley D., Beltra C., Gay A., Daubert J.C., Lecocq G., Poulain C., Cleland J.G.F.C., Shelton R., Lip G.Y.H., Choudhury A., Abuladze G., Jashi I., Cokkinos D.V., Tsiavou A., Giamouzis G., Dagres N., Kostopoulou A., Domproglou, Tsoutsani, Stefanadis Ch., Latsios G., Vogiatzis I., Gotsis A., Bozia P., Karakiriou M., Koulouris S., Parissis J., Kostakis G., Kouris N., Kontogianni D., Athanasios K., Douras A., Tsanakis T., Marketou M., Patsourakos N., Czopf L., Halmosi R., Preda I., Csoti E., Badics A., Strasberg B., Freedberg N.A., Katz A., Zalzstein E., Grosbard A., Goldhammer E., Nahir M., Epstein M., Vider I., Luria D., Mandelzweig L., Aloisi B., Cavallaro A., Antonielli E., Doronzo B., Pancaldo D., Mazzola C., Buontempi L., Calvi V., Giuffrida G., Figlia A., Ippolito F., Gelmini G.-P., Gaibazzi N., Ziacchi V., De Tommasi F., Lombardi F., Fiorentini C., Terranova P., Maiolino P., Albunni M., Pinna-Pintor P., Fumagalli S., Masotti G., Boncinelli L., Rossi D., Santoro G.M., Fioranelli M., Naccarella F., Maranga S.S., Lepera G., Bresciani B., Seragnoli E., Forti M.C., Cortina V., Baciarello G., Cicconetti P., Lax A., Vitali F., Igidbashian D., Scarpino L., Terrazzino S., Cantu F., Pentimalli F., Novo S., Coppola G., Zingarini G., Ambrozio G., Moruzzi P., Callegari S., Saccomanno G., Russo P., Carbonieri E., Paino A., Zanetta M., Barducci E., Cemin R., Rauhe W., Pitscheider W., Meloni M., Marchi S.M., Di Gennaro M., Calcagno S., Squaratti P., Quartili F., Bertocchi P., De Martini M., Mantovani G., Komorovsky R., Desideri A., Celegon L., Tarantini L., Catania G., Lucci D., Bianchini F., Puodziukynas A., Kavoliuniene A., Barauskiene V., Aidietis A., Barysiene J., Vysniauskas V., Zukauskiene I., Kazakeviciene N., Georgievska-Ismail L., Poposka L., Vataman E., Grosu A.A., Scholte Op Reimer W., De Swart E., Lenzen M., Jansen C., Brons R., Tebbe H., Van Hoogenhuyze D.C.A., Veerhoek M.J., Kamps M., Haan D., Van Rijn N., Bootsma A., Baur L., Van Den Dool A., Fransen H., Eurlings L., Meeder J., De Boer M.J., Winter J., Broers H., Werter C., Bijl M., Versluis S., Milkowska M., Wozakowska-Kaplon B., Janion M., Lepska L., Swiatecka G., Kokowicz P., Cybulski J., Gorecki A., Szulc M., Rekosz J., Manczak R., Wnuk-Wojnar A.-M., Trusz-Gluza M., Rybicka-Musialik A., Myszor J., Szpajer M., Cymerman K., Sadowski J., Sniezek-Maciejewska M., Ciesla-Dul M., Gorkiewicz-Kot I., Grodzicki T., Rewiuk K., Kubik L., Lewit J., De Sousa J.M.F.R., Ferreira R., Freitas A., Morais J.C.A., Pires R., Veloso Gomes M.J., Gago P., Candeias R.A.C., Nunes L., Miranda Sa J.V., Ventura M., De Oliveira M., Alves L.B., Bostaca I., Olariu C.T., Dan G.A., Dan A., Podoleanu C., Frigy A., Georgescu G.I.M., Arsenescu C., Statescu C., Sascau R., Dimitrascu D.L., Rancea R., Shubik Y.V., Duplyakov D., Shalak M., Danielyan M., Galyavich A., Zakirova V., Hatala R., Kaliska G., Kmec J., Zupan I., Tasie J., Vokac D., Edvardsson N., Poci D., Gamra H., Denguir H., Sepetoglu A., Arat-Ozkan A., Orynchak M., Paliy E., Vakalyuk I., Malidze D., Prog R., Yabluchansky M.I., Makienko N.V., Potpara T., Knezevic S., and Randjelovic M.

Subjects
Adult, Heart Failure, Male, Rate control, Risk Factor, Cardiology, Coronary Artery Disease, Guideline, Middle Aged, Atrial fibrillation, Europe, Stroke, Anticoagulation, Prospective Studie, Anti-Arrhythmia Agent, Echocardiography, Hypertension, Practice Guidelines as Topic, Rhythm control, Female, Societies, Medical, Aged, Human
Abstract

Aims To describe atrial fibrillation (AF) management in member countries of the European Society of Cardiology (ESC) and to verify cardiology practices against guidelines. Methods and results Among 182 hospitals in 35 countries, 5333 ambulant and hospitalized AF patients were enrolled, in 2003 and 2004. AF was primary or secondary diagnosis, and was confirmed on ECG in the preceding 12 months. Clinical type of AF was reported to be first detected in 978, paroxysmal in 1517, persistent in 1167, and permanent in 1547 patients. Concomitant diseases were present in 90% of all patients, causing risk factors for stroke to be also highly prevalent (86%). As many as 69% of patients were symptomatic at the time of the survey; among asymptomatic patients, 54% were previously experienced symptoms. Oral anticoagulation was prescribed in 67 and 49% of eligible and ineligible patients, respectively. A rhythm control strategy was applied in 67% of currently symptomatic patients and in 44% of patients who never experienced symptoms. Conclusion This survey provides a unique snapshot of current AF management in ESC member countries. Discordance between guidelines and practice was found regarding several issues on stroke prevention and antiarrhythmic therapy.

Published
2005

Catalog

Books, media, physical & digital resources
See catalog results