General Cardiology
Cardiology 1992;81:233-237
Department of Biomedical Science and Human Oncology, Section of Internal Medicine, Chair of Medical Therapy, University of Bari Medical School, Bari, Italy
K e y w o rd s
Cigarette smoking Normotension Hypertension Blood pressure variability Heart rate Finapres Ambulatory monitoring
Cardiovascular Effects of Cigarette Smoking
A b stra ct
The risk of cardiovascular morbidity and mortality is greatly affected by cigarette smoking. In order to study the pressor response to smoking. 10 normotensive and 10 mild or moder ate essential-hypertensive smokers (> 20 cigarettes daily) were compared with 2 comparable groups of non-smokers. All sub jects were asked to smoke 4 cigarettes during 1 h; blood pres sure (BP) and heart rate (HR) were monitored beat-to-beat by a non-invasive device (Finapres Ohmeda) during the smoking period and during the immediately preceding non-smoking hour. Furthermore, all subjects underwent 24-hour ambula tory BP monitoring. In all groups, each cigarette induced a similar and statistically significant increase from baseline for both BP and HR. The recovery from the marked rise in BP and HR was very slow so that in the smoking hours BP and HR were persistently higher than in non-smoking hours; there were no statistically significant differences between the four groups. During 24-hour ambulatory monitoring both normoand hypertensive smokers showed higher BP values and higher BP variability in comparison with the respective nonsmokers’ group. In conclusion, smoking habits were associ ated with a persistent increase in BP in each group we studied, possibly contributing to a smoking-related cardiovascular risk.
Introduction
Higher rates of cardiovascular disease and premature mortality have been reported for cigarette smokers in many prospective studies
Received: May 23, 1992 Accepted: May 26. 1992
[ 1]. Epidemiological data have indicated that cigarette smoking and hypertension are major risk factors in the development of cardiovas cular disease [2],
Dr. Giuseppe Ranieri Department of Biomedical Science anc Human Oncology Section of Internal Medicine, Chair of Medical Therapy University of Bari Medical School, Policlinico Piazza G. Cesare. 11 .1-70124 Bari (Italy)
© 1992 S. Kargcr AG, Basel 0008-6312/92/ 0815—023352.75/0
Downloaded by: King's College London 137.73.144.138 - 2/2/2018 9:13:28 AM
Raffaele De Cesaris Giuseppe Ranieri Vincenzo Filitti Massimo Vincenzo Bonfantino Antonia Andriani
234
M ethods In this study 40 patients were recruited: 10 normotensive non-smokers, 10 normotensive smokers, 10 hy pertensive non-smokers and 10 hypertensive smokers. Written consent was obtained from all patients according to international regulations. The four groups were well matched for age, sex and weight, and all were white-collar workers. The two hypertensive groups also showed a comparable dura tion and baseline severity of hypertension. Hypertensive patients had mild to moderate essen tial sustained hypertension. Sustained hypertension was documented by an average of three successive sit ting diastolic-pressure measurements between 95 and 114 mm Hg (Korotkoff phase V) on at least three sepa rate out-patient visits. Previous antihypertensive med ication. if any, was stopped at least 4 weeks before the start of the study. The complete diagnosis of essential hypertension was based on history, results of physical examination and appropriate laboratory tests. The smokers smoked the same brand of cigarettes and had smoked a minimum of 20 cigarettes per day for at least 5 years. This brand was used in the study. The nonsmokers had never smoked. None of the patient had cardiac, hepatic or renal involvement. Systemic arterial blood pressure was measured by a mercury sphygmomanometer. All sub jects underwent a 2-hour beat-to-beat blood pressure and heart rate recording and a 24-hour ambulatory' blood pressure monitoring. Beat-to-beat measurements were made by a noninvasive finger device (Finapres 2300: Ohmeda. Engle wood, Colo., USA) which produces beat-to-beat values similar to those obtained by intra-arterial monitoring [ 12]; blood pressure and heart rate were measured for 2 h and recorded using a customized software pro gram. Smokers had not smoked for 12 h. Measurements were made in the control condition ( 1 h) and during a period in which subjects were asked to smoke 4 cigarettes, one every 15 min. The subjects lay supine for a 2-hour recording peri od. The cigarettes were of the filter type, with a nico tine content of 1.2 mg per cigarette. Within a 3-day period after the Finapres test the subjects underwent 24-hour ambulatory blood pres sure monitoring, using the SpaccLabs device (model 90207; Redmond. Wash.. USA). Blood pressure was measured every 15 min from 6.00 to midnight and every 20 min from midnight to 6.00. Monitoring was carried out on a work day. Daytime was arbitrarily defined as being from 7.00 to 22.00. and nighttime from 22.00 to 7.00.
De Cesaris/Ranieri/Filitti/Bonfaiitino/ Andriani
Cardiovascular Response to Smoking
Downloaded by: King's College London 137.73.144.138 - 2/2/2018 9:13:28 AM
Further evidence suggests that cigarette smoking interacts with hypertension to in crease the risk of cardiovascular disease [2]. Moreover, cigarette smoking increases the cardiovascular risk of hypertension in partic ular, for any level of systolic or diastolic blood pressure [2], The acute haemodynamic response to ciga rette smoking includes an increase in the heart rate, systolic and diastolic arterial pres sure and myocardial contractility [3-7]. Car diac output rises primarily as a result of the increase in the heart rate. The elevation in arterial pressure is caused by increases in both cardiac output and systemic vascular resis tance. Furthermore, some studies have reported that blood pressure and body weight are higher in non-smokers than in smokers [8, 9], and this weight difference is believed to ex plain the lower blood pressure reported in smokers. Within 1 min of starting to smoke, the heart rate begins to increase and may rise by 30% during the First 10 min of smoking. It may begin to decrease as smoking continues, but does not return to the resting value imme diately after smoking has ceased. Blood pres sure tends to follow the same trend as heart rate [10]. Therefore, it is possible that in heavy smokers, blood pressure is steadily ele vated rather than reduced. Moreover, Groppelli et al. [11] reported that repeated episodes of smoking determine a persistent blood pressure increase, and that there is no short-term tolerance to the effects of smoking. To explore these apparently contradictory findings we studied the effects of cigarette smoking on blood pressure and heart rate in four different classes of subjects: normotensive habitual smokers and non-smokers, and hypertensive habitual smokers and nonsmokers.
Normotensive non-smokers 210
210
180 -
180
150
150
O) 120
x I
Normotensive smokers
90 60 30 -
I dl dl dl J i l l o> 120
X
I
90-
6030
1st
2nd
3rd
4th
1st
2nd
3rd
Cigarettes smoked
Cigarettes smoked
Hypertensive non-smokers
Hypertensive smokers
4th
240 -| 210 180 150
^ E
120 90.-
Idol
60 30 0
1st
2nd
3rd
4th
1st
Cigarettes smoked
2nd
3rd
4th
Cigarettes smoked
Fig. 1. Systolic and diastolic blood pressure before and during smoking in the four groups of subjects. Measurements were averaged over all subjects of each group and the 15-min means ( ± SD) are shown. □ = control; ■ = smoking. * p < 0.05, ** p < 0 .0 1, *** p < 0.001, control versus smoking.
Results
The changes in average systolic and dia stolic blood pressure before and after the peak effects of smoking a cigarette are shown in fig ure l. In each group, systolic and diastolic blood pressure and heart rate increased markedly after the first cigarette smoked. The peak was
Downloaded by: King's College London 137.73.144.138 - 2/2/2018 9:13:28 AM
The 24-hour blood pressure SD was taken as a mea sure of blood pressure variability. Both groups of smokers smoked their usual daily number of cigarettes during the 24-hour blood pres sure monitoring. Smoking-induced changes during the Finapres test were evaluated by one-way analysis of variance and the Bonfcrroni test. The unpaired t test was used to evaluate differences between the groups. Values are presented as the mean ± SD, and the level of significance was taken as p < 0.05.
Table 1. Results of 24-hour ambulator)' blood pressure monitoring in four study groups
Mean blood pressure, mm Hg
SD
day
night
day
night
90 ± 9 98 ±8* 114 ± 9 126 ±8**
79 + 7 82 ± 6 103 ± 9 104 ± 10
6.0±0.2 7.4 + 0.2*** 8.1 ±0.2 9.0 ±0.3***
4.8 ±0.2 4.9 ±0.3 6.6±0.2 6.7 ±0.2
Normotensive non-smokers Normotensive smokers Hypertensive non-smokers Hypertensive smokers
* p < 0.05. * * p < 0 .0 1 .* * * p < 0.001. versus the respective non-smoking group.
236
D iscussion
Compared with non-smokers, tobacco smokers have at least twice the risk of cardio vascular complications, including myocardial infarction, sudden death and stroke. Smoking only a few cigarettes a day substantially in creases the cardiovascular risk [ 1]. The combination of hypertension and smoking further increases the risk of cardio vascular events. Our data show that during heavy smoking, blood pressure and the heart rate are steadily increased, and emphasize that smoking does not induce tolerance [13]. This finding is present in all subjects we have studied (normotensive non-smokers, normotensive habitual smokers, hypertensive nonsmokers and hypertensive habitual smokers). These data suggest that in previous studies [8] smokers probably had reduced blood pressure values because blood pressure measurements were assessed after a period of abstinence from smoking, and therefore did not repre sent the subjects’ usual blood pressure. Another important finding is that both the normotensive and the hypertensive smokers in the present study showed higher mean blood pressure values during the day and higher SDs around the mean, that is an in creased variability, in comparison with their respective non-smoker groups.
Dc Cesaris/Ranieri/Filitti/Bonlartino/ Andriani
Cardiovascular Response lo Smoking
Downloaded by: King's College London 137.73.144.138 - 2/2/2018 9:13:28 AM
reached after 2.5 tnin. The following three cig arettes induced similar peak values of blood pressure and heart rate. These findings suggest that repeated smok ing induces constant effects on blood pressure and heart rate, without attenuation. Figure l shows that smoking induces a lasting and con tinuous increase in average systolic and dia stolic blood pressure, and heart rate. Recov ery from the marked rise in blood pressure and heart rate induced by each cigarette was very slow, so that baseline pre-smoking values were progressively higher after each cigarette smoked. In all groups the baseline values for the sec ond cigarette were significantly higher com pared with the first cigarette (p < 0.001). The blood pressure monitoring showed higher daytime mean blood pressure values and vari ability (average SDs of mean blood pressure) in both the normo- and hypertensive smokers compared with the respective non-smoker groups (table 1). At night these parameters showed no significant differences between the groups. The heart rate, also, showed no signif icant differences between the groups, neither by day nor by night.
Therefore, smoking in itself might consti tute a cardiovascular risk by acting upon blood pressure, in addition to its effects on lipid metabolism [14-16] and haemostatic function [17. 18]. Furthermore, by increasing blood pressure variability, smoking increases the cardiovas cular risk, since it is well know that increased
blood pressure variability in hypertensives is related to target organ damage [ 19, 20], These Findings may provide some impor tant explanations as to the mechanisms of smoking-induced cardiovascular risk. Giving up cigarette smoking should be rec ommended for the general population, but particularly for hypertensive patients.
References 8 Wilhemsen L: Coronary heart dis ease: Epidemiology of smoking and intervention studies of smoking. Am Heart.I 1988:115:242-249. 9 Karvoncn M. Orma E. Keys A. Fidanza S. Broz.ek J: Cigarette smok ing. scrum cholesterol, blood pres sure and body fatness: Observation in Finland. Lancet 1959:i:492-496. 10 Trap-Jensen J. Carlsen JE. Svendsen TL. Christensen NJ: Car diovascular and adrenergic effects of cigarette smoking during imme diate non-sclectivc beta-adrcnoceptor blockade in humans. Eur .1 Clin Invest 1979:9:181-183. 11 Grappelli A, Omboni S. Parati G. Mancia G: Blood pressure and heart rate response to repeated smoking before and after beta-blockade and selective alpha-1 inhibition. J Hypertens 1990:8(suppl 5):S35-S40. 12 Parati G. Casadei R. Grappelli A. Di Rienzo M. Mancia G: Compari son of finger and intra-arterial blood pressure monitoring at rest and dur ing laboratory' testing. Hypertension 1989:13:647—655. 13 Benowitz NL. Jacob P III. Jones RT. Rosenberg J: Interindividual variability in the metabolism and cardiovascular effects of nicotine in man. J Pharmacol Exp Thcr 1982: 221:368-372. 14 Garrison RJ. Kannel WB. Feinleib M. Castelli WP. McNamara PM. Padgett SJ: Cigarette smoking and HDL cholesterol: The Framingham offspring study. Atherosclerosis 1978;30:17-25."
15 Williams P. Robinson D. Bailey A: High-density lipoprotein and coro nary risk factors in normal men. Lancet 1979;i:72—75. 16 Criqui MIL Wallace RB. Heiss G. Mishkel M. Schonfeld G. Jones GT: Cigarette smoking and plasma highdensity lipoprotein cholesterol: The Lipid Research Clinics Program Prevalence Study. Circulation 1980: 62(suppl IV):70—76. 17 Kannel WB. Dagostino RB. Belan ger AJ: Fibrinogen, cigarette smok ing and risk of cardiovascular dis ease: Insights from the Framingham Study. Am Heart J 1987:113:10061010.
18 Haire W'D. Goldsmith JC. Ras mussen J: Abnormal fibrinolysis in healthy male cigarette smokers: Role of plasminogen activator in hibitors. Am J Hematol 1989:31: 36-40. 19 Parati G. Pomidossi G. Albini F. Malaspina D. Mancia G: Relation ship of 24-hour blood pressure mean and variability to severity of targetorgan damage in hypertension. J Hypertens 1987:5:93-98. 20 Pcssina AC. Palatini P. Sperti G: Evaluation of hypertension and re lated target organ damage by aver age day-time blood pressure. Clin Exp Hypertens [A] 1985:7:267— 271.
237
Downloaded by: King's College London 137.73.144.138 - 2/2/2018 9:13:28 AM
1 Kännel WB. McGee DL. Castelli WP: Latest perspectives on cigarette smoking and cardiovascular disease: The Framingham Study. J Cardiac Rehab 1984:4:267-277.' 2 Kannel WB: Contributions of the Framingham Study to the conquest of coronary artery disease. Am J Cardiol 1988;62:1109-1112. 3 Cryer PE. Haymond MW, Santiago JV. Shah SD: Norepinephrine and epinephrine release and adrenergic mediation of smoking-associated hemodynamic and metabolic events. N Engl J Med 1976:295: 573-577. 4 Nicod P. Rehr R. Winniford MD. Campbell WB. Firth BG. Hillis LD: Acute systemic and coronary hemo dynamic and serologic responses to cigarette smoking in long-term smokers with atherosclerotic coro nary artery' disease. J Am Coll Car diol 1984:4:964-971. 5 Koch A. Hoffman K. Steck W: Acute cardiovascular reactions after cigarette smoking. Atherosclerosis 1980:35:67-75. 6 Rabinowitz BD. Thorp K. Huber GL, Abelmann WH: Acute hemody namic effects of cigarette smoking in man assessed by systolic time inter vals and echocardiography. Circula tion 1979:60:752-760. 7 Thomas CB. Bateman J. Lindrberg E. Bornhold H: Observation on the individual effects of smoking on the blood pressure, heart rate, stroke volume and cardiac output of healthy young adults. Ann Intern Med 1956:44:874-892.
Cardiology 1992;81:233-237
Department of Biomedical Science and Human Oncology, Section of Internal Medicine, Chair of Medical Therapy, University of Bari Medical School, Bari, Italy
K e y w o rd s
Cigarette smoking Normotension Hypertension Blood pressure variability Heart rate Finapres Ambulatory monitoring
Cardiovascular Effects of Cigarette Smoking
A b stra ct
The risk of cardiovascular morbidity and mortality is greatly affected by cigarette smoking. In order to study the pressor response to smoking. 10 normotensive and 10 mild or moder ate essential-hypertensive smokers (> 20 cigarettes daily) were compared with 2 comparable groups of non-smokers. All sub jects were asked to smoke 4 cigarettes during 1 h; blood pres sure (BP) and heart rate (HR) were monitored beat-to-beat by a non-invasive device (Finapres Ohmeda) during the smoking period and during the immediately preceding non-smoking hour. Furthermore, all subjects underwent 24-hour ambula tory BP monitoring. In all groups, each cigarette induced a similar and statistically significant increase from baseline for both BP and HR. The recovery from the marked rise in BP and HR was very slow so that in the smoking hours BP and HR were persistently higher than in non-smoking hours; there were no statistically significant differences between the four groups. During 24-hour ambulatory monitoring both normoand hypertensive smokers showed higher BP values and higher BP variability in comparison with the respective nonsmokers’ group. In conclusion, smoking habits were associ ated with a persistent increase in BP in each group we studied, possibly contributing to a smoking-related cardiovascular risk.
Introduction
Higher rates of cardiovascular disease and premature mortality have been reported for cigarette smokers in many prospective studies
Received: May 23, 1992 Accepted: May 26. 1992
[ 1]. Epidemiological data have indicated that cigarette smoking and hypertension are major risk factors in the development of cardiovas cular disease [2],
Dr. Giuseppe Ranieri Department of Biomedical Science anc Human Oncology Section of Internal Medicine, Chair of Medical Therapy University of Bari Medical School, Policlinico Piazza G. Cesare. 11 .1-70124 Bari (Italy)
© 1992 S. Kargcr AG, Basel 0008-6312/92/ 0815—023352.75/0
Downloaded by: King's College London 137.73.144.138 - 2/2/2018 9:13:28 AM
Raffaele De Cesaris Giuseppe Ranieri Vincenzo Filitti Massimo Vincenzo Bonfantino Antonia Andriani
234
M ethods In this study 40 patients were recruited: 10 normotensive non-smokers, 10 normotensive smokers, 10 hy pertensive non-smokers and 10 hypertensive smokers. Written consent was obtained from all patients according to international regulations. The four groups were well matched for age, sex and weight, and all were white-collar workers. The two hypertensive groups also showed a comparable dura tion and baseline severity of hypertension. Hypertensive patients had mild to moderate essen tial sustained hypertension. Sustained hypertension was documented by an average of three successive sit ting diastolic-pressure measurements between 95 and 114 mm Hg (Korotkoff phase V) on at least three sepa rate out-patient visits. Previous antihypertensive med ication. if any, was stopped at least 4 weeks before the start of the study. The complete diagnosis of essential hypertension was based on history, results of physical examination and appropriate laboratory tests. The smokers smoked the same brand of cigarettes and had smoked a minimum of 20 cigarettes per day for at least 5 years. This brand was used in the study. The nonsmokers had never smoked. None of the patient had cardiac, hepatic or renal involvement. Systemic arterial blood pressure was measured by a mercury sphygmomanometer. All sub jects underwent a 2-hour beat-to-beat blood pressure and heart rate recording and a 24-hour ambulatory' blood pressure monitoring. Beat-to-beat measurements were made by a noninvasive finger device (Finapres 2300: Ohmeda. Engle wood, Colo., USA) which produces beat-to-beat values similar to those obtained by intra-arterial monitoring [ 12]; blood pressure and heart rate were measured for 2 h and recorded using a customized software pro gram. Smokers had not smoked for 12 h. Measurements were made in the control condition ( 1 h) and during a period in which subjects were asked to smoke 4 cigarettes, one every 15 min. The subjects lay supine for a 2-hour recording peri od. The cigarettes were of the filter type, with a nico tine content of 1.2 mg per cigarette. Within a 3-day period after the Finapres test the subjects underwent 24-hour ambulatory blood pres sure monitoring, using the SpaccLabs device (model 90207; Redmond. Wash.. USA). Blood pressure was measured every 15 min from 6.00 to midnight and every 20 min from midnight to 6.00. Monitoring was carried out on a work day. Daytime was arbitrarily defined as being from 7.00 to 22.00. and nighttime from 22.00 to 7.00.
De Cesaris/Ranieri/Filitti/Bonfaiitino/ Andriani
Cardiovascular Response to Smoking
Downloaded by: King's College London 137.73.144.138 - 2/2/2018 9:13:28 AM
Further evidence suggests that cigarette smoking interacts with hypertension to in crease the risk of cardiovascular disease [2]. Moreover, cigarette smoking increases the cardiovascular risk of hypertension in partic ular, for any level of systolic or diastolic blood pressure [2], The acute haemodynamic response to ciga rette smoking includes an increase in the heart rate, systolic and diastolic arterial pres sure and myocardial contractility [3-7]. Car diac output rises primarily as a result of the increase in the heart rate. The elevation in arterial pressure is caused by increases in both cardiac output and systemic vascular resis tance. Furthermore, some studies have reported that blood pressure and body weight are higher in non-smokers than in smokers [8, 9], and this weight difference is believed to ex plain the lower blood pressure reported in smokers. Within 1 min of starting to smoke, the heart rate begins to increase and may rise by 30% during the First 10 min of smoking. It may begin to decrease as smoking continues, but does not return to the resting value imme diately after smoking has ceased. Blood pres sure tends to follow the same trend as heart rate [10]. Therefore, it is possible that in heavy smokers, blood pressure is steadily ele vated rather than reduced. Moreover, Groppelli et al. [11] reported that repeated episodes of smoking determine a persistent blood pressure increase, and that there is no short-term tolerance to the effects of smoking. To explore these apparently contradictory findings we studied the effects of cigarette smoking on blood pressure and heart rate in four different classes of subjects: normotensive habitual smokers and non-smokers, and hypertensive habitual smokers and nonsmokers.
Normotensive non-smokers 210
210
180 -
180
150
150
O) 120
x I
Normotensive smokers
90 60 30 -
I dl dl dl J i l l o> 120
X
I
90-
6030
1st
2nd
3rd
4th
1st
2nd
3rd
Cigarettes smoked
Cigarettes smoked
Hypertensive non-smokers
Hypertensive smokers
4th
240 -| 210 180 150
^ E
120 90.-
Idol
60 30 0
1st
2nd
3rd
4th
1st
Cigarettes smoked
2nd
3rd
4th
Cigarettes smoked
Fig. 1. Systolic and diastolic blood pressure before and during smoking in the four groups of subjects. Measurements were averaged over all subjects of each group and the 15-min means ( ± SD) are shown. □ = control; ■ = smoking. * p < 0.05, ** p < 0 .0 1, *** p < 0.001, control versus smoking.
Results
The changes in average systolic and dia stolic blood pressure before and after the peak effects of smoking a cigarette are shown in fig ure l. In each group, systolic and diastolic blood pressure and heart rate increased markedly after the first cigarette smoked. The peak was
Downloaded by: King's College London 137.73.144.138 - 2/2/2018 9:13:28 AM
The 24-hour blood pressure SD was taken as a mea sure of blood pressure variability. Both groups of smokers smoked their usual daily number of cigarettes during the 24-hour blood pres sure monitoring. Smoking-induced changes during the Finapres test were evaluated by one-way analysis of variance and the Bonfcrroni test. The unpaired t test was used to evaluate differences between the groups. Values are presented as the mean ± SD, and the level of significance was taken as p < 0.05.
Table 1. Results of 24-hour ambulator)' blood pressure monitoring in four study groups
Mean blood pressure, mm Hg
SD
day
night
day
night
90 ± 9 98 ±8* 114 ± 9 126 ±8**
79 + 7 82 ± 6 103 ± 9 104 ± 10
6.0±0.2 7.4 + 0.2*** 8.1 ±0.2 9.0 ±0.3***
4.8 ±0.2 4.9 ±0.3 6.6±0.2 6.7 ±0.2
Normotensive non-smokers Normotensive smokers Hypertensive non-smokers Hypertensive smokers
* p < 0.05. * * p < 0 .0 1 .* * * p < 0.001. versus the respective non-smoking group.
236
D iscussion
Compared with non-smokers, tobacco smokers have at least twice the risk of cardio vascular complications, including myocardial infarction, sudden death and stroke. Smoking only a few cigarettes a day substantially in creases the cardiovascular risk [ 1]. The combination of hypertension and smoking further increases the risk of cardio vascular events. Our data show that during heavy smoking, blood pressure and the heart rate are steadily increased, and emphasize that smoking does not induce tolerance [13]. This finding is present in all subjects we have studied (normotensive non-smokers, normotensive habitual smokers, hypertensive nonsmokers and hypertensive habitual smokers). These data suggest that in previous studies [8] smokers probably had reduced blood pressure values because blood pressure measurements were assessed after a period of abstinence from smoking, and therefore did not repre sent the subjects’ usual blood pressure. Another important finding is that both the normotensive and the hypertensive smokers in the present study showed higher mean blood pressure values during the day and higher SDs around the mean, that is an in creased variability, in comparison with their respective non-smoker groups.
Dc Cesaris/Ranieri/Filitti/Bonlartino/ Andriani
Cardiovascular Response lo Smoking
Downloaded by: King's College London 137.73.144.138 - 2/2/2018 9:13:28 AM
reached after 2.5 tnin. The following three cig arettes induced similar peak values of blood pressure and heart rate. These findings suggest that repeated smok ing induces constant effects on blood pressure and heart rate, without attenuation. Figure l shows that smoking induces a lasting and con tinuous increase in average systolic and dia stolic blood pressure, and heart rate. Recov ery from the marked rise in blood pressure and heart rate induced by each cigarette was very slow, so that baseline pre-smoking values were progressively higher after each cigarette smoked. In all groups the baseline values for the sec ond cigarette were significantly higher com pared with the first cigarette (p < 0.001). The blood pressure monitoring showed higher daytime mean blood pressure values and vari ability (average SDs of mean blood pressure) in both the normo- and hypertensive smokers compared with the respective non-smoker groups (table 1). At night these parameters showed no significant differences between the groups. The heart rate, also, showed no signif icant differences between the groups, neither by day nor by night.
Therefore, smoking in itself might consti tute a cardiovascular risk by acting upon blood pressure, in addition to its effects on lipid metabolism [14-16] and haemostatic function [17. 18]. Furthermore, by increasing blood pressure variability, smoking increases the cardiovas cular risk, since it is well know that increased
blood pressure variability in hypertensives is related to target organ damage [ 19, 20], These Findings may provide some impor tant explanations as to the mechanisms of smoking-induced cardiovascular risk. Giving up cigarette smoking should be rec ommended for the general population, but particularly for hypertensive patients.
References 8 Wilhemsen L: Coronary heart dis ease: Epidemiology of smoking and intervention studies of smoking. Am Heart.I 1988:115:242-249. 9 Karvoncn M. Orma E. Keys A. Fidanza S. Broz.ek J: Cigarette smok ing. scrum cholesterol, blood pres sure and body fatness: Observation in Finland. Lancet 1959:i:492-496. 10 Trap-Jensen J. Carlsen JE. Svendsen TL. Christensen NJ: Car diovascular and adrenergic effects of cigarette smoking during imme diate non-sclectivc beta-adrcnoceptor blockade in humans. Eur .1 Clin Invest 1979:9:181-183. 11 Grappelli A, Omboni S. Parati G. Mancia G: Blood pressure and heart rate response to repeated smoking before and after beta-blockade and selective alpha-1 inhibition. J Hypertens 1990:8(suppl 5):S35-S40. 12 Parati G. Casadei R. Grappelli A. Di Rienzo M. Mancia G: Compari son of finger and intra-arterial blood pressure monitoring at rest and dur ing laboratory' testing. Hypertension 1989:13:647—655. 13 Benowitz NL. Jacob P III. Jones RT. Rosenberg J: Interindividual variability in the metabolism and cardiovascular effects of nicotine in man. J Pharmacol Exp Thcr 1982: 221:368-372. 14 Garrison RJ. Kannel WB. Feinleib M. Castelli WP. McNamara PM. Padgett SJ: Cigarette smoking and HDL cholesterol: The Framingham offspring study. Atherosclerosis 1978;30:17-25."
15 Williams P. Robinson D. Bailey A: High-density lipoprotein and coro nary risk factors in normal men. Lancet 1979;i:72—75. 16 Criqui MIL Wallace RB. Heiss G. Mishkel M. Schonfeld G. Jones GT: Cigarette smoking and plasma highdensity lipoprotein cholesterol: The Lipid Research Clinics Program Prevalence Study. Circulation 1980: 62(suppl IV):70—76. 17 Kannel WB. Dagostino RB. Belan ger AJ: Fibrinogen, cigarette smok ing and risk of cardiovascular dis ease: Insights from the Framingham Study. Am Heart J 1987:113:10061010.
18 Haire W'D. Goldsmith JC. Ras mussen J: Abnormal fibrinolysis in healthy male cigarette smokers: Role of plasminogen activator in hibitors. Am J Hematol 1989:31: 36-40. 19 Parati G. Pomidossi G. Albini F. Malaspina D. Mancia G: Relation ship of 24-hour blood pressure mean and variability to severity of targetorgan damage in hypertension. J Hypertens 1987:5:93-98. 20 Pcssina AC. Palatini P. Sperti G: Evaluation of hypertension and re lated target organ damage by aver age day-time blood pressure. Clin Exp Hypertens [A] 1985:7:267— 271.
237
Downloaded by: King's College London 137.73.144.138 - 2/2/2018 9:13:28 AM
1 Kännel WB. McGee DL. Castelli WP: Latest perspectives on cigarette smoking and cardiovascular disease: The Framingham Study. J Cardiac Rehab 1984:4:267-277.' 2 Kannel WB: Contributions of the Framingham Study to the conquest of coronary artery disease. Am J Cardiol 1988;62:1109-1112. 3 Cryer PE. Haymond MW, Santiago JV. Shah SD: Norepinephrine and epinephrine release and adrenergic mediation of smoking-associated hemodynamic and metabolic events. N Engl J Med 1976:295: 573-577. 4 Nicod P. Rehr R. Winniford MD. Campbell WB. Firth BG. Hillis LD: Acute systemic and coronary hemo dynamic and serologic responses to cigarette smoking in long-term smokers with atherosclerotic coro nary artery' disease. J Am Coll Car diol 1984:4:964-971. 5 Koch A. Hoffman K. Steck W: Acute cardiovascular reactions after cigarette smoking. Atherosclerosis 1980:35:67-75. 6 Rabinowitz BD. Thorp K. Huber GL, Abelmann WH: Acute hemody namic effects of cigarette smoking in man assessed by systolic time inter vals and echocardiography. Circula tion 1979:60:752-760. 7 Thomas CB. Bateman J. Lindrberg E. Bornhold H: Observation on the individual effects of smoking on the blood pressure, heart rate, stroke volume and cardiac output of healthy young adults. Ann Intern Med 1956:44:874-892.
