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6. The chronic effects of cannabis use on health
6.3 Cardiovascular effects
Both the inhalation of marijuana smoke and the ingestion of THC reliably produces an increase in heart rate of 20 per cent to 50 per cent over baseline (Huber et al, 1988; Jones, 1984). When cannabis is smoked, the heart rate increases within two to three minutes, peaks within 15 to 30 minutes, and may remain elevated for up to two hours. When ingested, these effects are delayed for several hours, and last for four to five hours (Maykut, 1984). There are also complex changes in blood pressure which depend upon posture: blood pressure is increased while the person is sitting or lying, but decreases on standing, so that a sudden change from a recumbent to an upright position may produce postural hypotension and, in extreme cases, fainting (Maykut, 1984).
Young, healthy hearts are likely to be only mildly stressed by these acute effects of cannabis (Tennant, 1983). The clinical significance of the repeated occurrence of these effects in chronic heavy cannabis users remains uncertain, because there is evidence from clinical and experimental studies (Benowitz and Jones, 1975; Jones and Benowitz, 1976; Nowlan and Cohen, 1977) that tolerance develops to the acute cardiovascular effects of cannabis. Clinical studies employing chronic dosing over periods of up to nine weeks show that the increased heart rate all but disappears, while the blood pressure increase is much attenuated. Tolerance to the cardiovascular effects develops within seven to 10 days in persons receiving high daily doses by the oral route (Jones, 1984).
The field studies of chronic heavy users in Costa Rica (Carter et al, 1980), Greece (Stefanis et al, 1977), and Jamaica (Rubin and Costas, 1975) failed to disclose any evidence of cardiac toxicity, even in those subjects with heart disease that was unrelated to their cannabis use. The findings of the field studies have been supported by the fact that electrocardiographic studies in conditions of both acute and prolonged administration have rarely revealed pathological changes (Benowitz and Jones, 1975; Jones, 1984). It seems reasonable to conclude then that among healthy young adults who use cannabis intermittently, cannabis use is not a major risk factor for life-threatening cardiovascular events in the way that the use of cocaine and other psychostimulants can be (Gawin and Ellinwood, 1988). There is suggestive evidence of a small risk, however, since there have been a number of case reports of myocardial infarction in young men who were heavy cannabis smokers and had no personal history of heart disease (Tennant, 1983; Choi and Pearl, 1989; Pearl and Choi, 1992; Podczeck et al, 1990). Such cases deserve close investigation to exclude the role of other cardiotoxic drugs.
The possibility remains that chronic heavy cannabis smoking may have more subtle effects on the cardiovascular system. Jones (1984) has suggested, for example, that there is a possibility that "after years of repeated exposure" there may be "lasting, perhaps even permanent, alterations of the cardiovascular system function" (p331). Arguing by analogy with the long-term cardiotoxic effects of tobacco smoking, he suggests that there are "enough similarities between THC and nicotine cardiovascular effects to make the possibility plausible" (p331). Moreover, since many cannabis smokers are also cigarette smokers, there is the possibility that there may be adverse interactions between nicotine and cannabinoids in their effects on the cardiovascular system.
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6.3.1 Effects on patients with cardiovascular disease
The cardiovascular effects of cannabis may adversely affect patients with pre-existing cardiovascular disease. As the Institute of Medicine observed:
the possibility is great that the abnormal heart and circulation will not be as tolerant of an agent that speeds up the heart, sometimes unpredictably raises or drops blood pressure, and modifies the activities of the autonomic nervous system (pp69-70).
There are a number of concerns about the potentially deleterious effects of cannabis use on patients with ischaemic heart disease, hypertension, and cerebrovascular disease (Jones, 1984; National Academy of Science, 1982). First, THC appears to increase the production of catecholamines which stimulate the activity of the heart, thereby increasing the risk of cardiac arrhythmias in susceptible patients. Second, THC increases heart rate, thereby producing chest pain (angina pectoris) in patients with ischaemic heart disease, and perhaps increasing the risk of a myocardial infarction. Third, THC also has analgesic properties (see below p194) which may attenuate chest pain, delaying treatment seeking, and thereby perhaps increasing the risk of fatal arrhythmias. Fourth, marijuana smoking increases the level of carboxyhaemoglobin, thereby decreasing oxygen delivery to the heart, increasing the work of the heart and, perhaps, the risk of atheroma formation. Moreover, the reduced delivery of oxygen to the heart is compounded by a concomitant increase in the work of the heart - and therefore its oxygen requirements - because of the tachycardia induced by THC. Fifth, patients with cerebrovascular disease may be put at risk of experiencing strokes by unpredictable changes in blood pressure, and patients with hypertension may experience exacerbations of their disease for the same reason.
After considering the known cardiovascular effects of THC, and their likely interactions with cardiovascular disease, the Institute of Medicine (1982) concluded that it: " ... seems inescapable that this increased work, coupled with stimulation by catecholamines, may tax the heart to the point of clinical hazard" (p70). Despite the plausibility of the reasoning, there is very little direct evidence of the adverse effects of cannabis on persons with heart disease (Jones, 1984). Among the few relevant pieces of research evidence are two laboratory studies of the acute cardiovascular effects of smoking marijuana cigarettes on patients with occlusive heart disease. Aronow and Cassidy (1974) conducted a double blind placebo control study comparing the effect on heart rate and the time required to induce chest pain during an exercise tolerance test, of smoking a single marijuana cigarette containing 20mg of THC, with the effect of a placebo marijuana cigarette. Heart rate increased by 43 per cent, and the time taken to produce chest pain was approximately halved, after smoking a marijuana cigarette. It appeared that cannabis increased the myocardial oxygen demand while reducing the amount of oxygen delivered to the heart (Aronow and Cassidy, 1974).
Aronow and Cassidy (1975) compared the effects of smoking a single marijuana cigarette and a high nicotine cigarette in 10 men with occlusive heart disease, all of whom were 20 a day cigarette smokers. A 42 per cent increase in heart rate was observed after smoking the marijuana cigarette compared with a 21 per cent increase after smoking the tobacco cigarette. Exercise tolerance time was halved (49 per cent) after smoking a marijuana cigarette by comparison with a 23 per cent decline after smoking a tobacco cigarette.
Apart from these studies, there is very little direct evidence on the risks of cannabis use by persons with cardiovascular disease. The reasons for the absence of adverse effects of chronic cannabis use on diseased cardiovascular systems are unclear. It should not be assumed in the absence of evidence, however, that such effects do not exist. The absence of evidence may simply reflect the lack of systematic study. It may be that the development of tolerance to the cardiovascular effects with chronic heavy dosing has protected the heaviest users from experiencing such effects: it may be that there has been an insufficient exposure to cannabis smoking of a sufficiently large number of vulnerable individuals (National Academy of Science, 1982); or it may be that cardiologists have missed any such evidence because they have not inquired about cannabis use among their patients.
On the face of it, the possibility of cannabis smokers developing heart disease may seem "theoretical". Most cannabis users are healthy young adults who smoke intermittently, most discontinue their use by their late 20s, and very few of the minority who become heavy cannabis users are likely to have clinical occlusive heart disease or other atherosclerotic disease. But the possibility of such adverse effects is not entirely theoretical.
First, any such effects would contraindicate the therapeutic uses of cannabinoids among older patients, such as those with cancer and glaucoma, who are at higher risk, because they are older, of having significant heart disease (Jones, 1984).
Second, the chronic heavy cannabis users who were inducted into cannabis use in the late 1960s and early 1970s are now entering the period in which that minority who have continued to smoke cannabis are at risk of experiencing symptoms of clinical heart disease. Among this group cannabis use may contribute to an earlier expression of heart disease, especially, if they have also been heavy cigarette smokers. Because of the high rates of cessation of cannabis use with age, however, this may be such a small number of persons that the effect is difficult to detect clinically, especially if cannabis use is not considered to be a risk factor about which cardiologists systematically inquire. It may be worth exploring this possibility by including questions on cannabis use in case-control studies of cardiovascular disease among middle-aged adults.
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On the available evidence, it is still appropriate to endorse the conclusions reached by the expert committee appointed by the National Academy of Science in 1982 that, although the smoking of marijuana "causes changes to the heart and circulation that are characteristic of stress ... there is no evidence ... that it exerts a permanently deleterious effect on the normal cardiovascular system..." p72). The situation may be less benign for those with "abnormal heart or circulation" since there is evidence that marijuana poses "a threat to patients with hypertension, cerebrovascular disease and coronary atherosclerosis" (p72) by increasing the work of the heart. The "magnitude and incidence" of the threat remains to be determined as the cohort of chronic cannabis users of the late 1960s enters the age of maximum risk for complications of atherosclerosis of the cardiac, brain and peripheral vessels. In the interim, because any such effects could be life threatening in patients with significant occlusion of the coronary arteries or other cerebrovascular disease, such persons should be advised not to smoke cannabis (Tennant, 1983).