Responses collected during the most recent interview were used for these analyses.To examine the dimensionality of the 13 subjective experiences examined for each substance, we conducted Mokken Scale Analysis using the statistical software STATA.Mokken scaling analysis extends traditional factor analysis by systematically hierarchically ordering items that are highly correlated. Mokken analysis provides a nonparametric, iterative scale-building technique that identifies the smallest set of internally consistent scales from a given item pool. This model assumes the presence of one or more latent traits that can be measured by subject responses to a set of items.MSA is probabilistic and hierarchical, meaning that the items can be ordered by a degree of “difficulty”;individuals who agree with a more difficult item will tend to agree with less difficult items.Scales from MSA are formed by taking pairs of items with the highest correlation and including other items until there is no further improvement.Loevinger’s H coefficients, which indicate the fit of an item to the scale, are computed for each item within a scale and for the scale as a whole.H coefficients ranging between 0.3 and 0.4 indicate a weak scale, 0.4–0.5 a medium scale, and 0.5–0.9 a strong scale. In MSA, an item can remain “unscaled” because it could not be added to one of the alternative scales without weakening the scale’s homogeneity. Based on our previous analyses,we used the scaling derived from the CADD sample. Positive and negative scales were standardized by age, sex, and clinical status with two groups.Pairwise correlations between the resulting two scales were then determined for alcohol, tobacco,pot drying and marijuana.In the current report, we examined subjective experiences to three commonly used drugs of abuse among young adults from the general community and an area treatment program.
In these data, we obtained results that supported previous observations indicating positive and negative subjective experiences for a particular drug were predictive of problem use of that same drug. We then extended this relationship in two ways. First, we obtained results that supported the notion that positive and negative experiences to one drug are similar to those experienced for another drug and second, that subjective experiences to a drug are predictive of the risk for problem use of other drugs. We interpret these findings to suggest that subjective experiences may be a useful indicator of a common liability towards use and problem use of multiple substances. Following on our previous work on marijuana and subjective experiences,we used Mokken scaling to simultaneously examine whether subjective experiences to three drugs are associated with drug use outcomes. From these analyses we observed that the subjective experience scales for each of the three drugs were comparable to those found in previous studies despite using a different methodology.We observed differences in item means and hierarchical ordering of the items by substance suggesting that subjects are reporting drug specific subjective experiences. This interpretation is consistent with findings from laboratory based studies which have shown that subjects can differentiate between a placebo and a drug or between different drugs based on subjective experiences.As different combinations of alcohol, tobacco, and marijuana use are commonly reported in epidemiological studies, we investigated the relationship between subjective experiences to different drugs in poly-substance users. We observed that subjective experiences to one drug were significantly correlated with experiences to another drug, though the strength of the relationship varied for different drug combinations. The strongest relationships were between alcohol and marijuana, replicating two previous studies,and between alcohol and tobacco. These particular drug combinations target similar neuronal receptor systems and are reported to enhance the overall drug experience when taken together.Further, as subjective experiences are thought to reflect the underlying physiology of a drug’s actions,these cross-substance relationships may provide a closer approximation of a common risk factor suitable for molecular genetic investigation. In this sample of community and clinical subjects, subjective experiences for one drug were associated with outcomes related to a different drug. Though our results replicate findings that relate positive experiences with greater use of other drugs, we also identified that negative experiences were predictive of abuse and dependence status of a different drug. In particular, negative effects of alcohol and marijuana were associated with misuse of these same drugs as well as tobacco. Although this may appear counter-intuitive, a possible explanation could be that subjects who needed greater amounts of a drug in order to feel its effects drove the observed association.
Findings from laboratory-based drug discrimination studies suggest that some subjects are unable to differentiate between drug and placebo at a standard training dose.Differences between the two conditions could, however, be reported as non-discriminators were exposed to greater doses of a drug. Interestingly, those who were able to discriminate between non-exposure and exposure to a drug reported stronger positive and negative subjective experiences, often simultaneously,at greater doses. This underscores the importance of dose in determining individuals’ drug sensitivity as assessed by subjective experiences. The relationship between drug dose, the resulting subjective experiences, and problem drug use has also been examined using self-ratings to the effects of alcohol [SRE; 28]. The SRE primarily assesses negative experiences to alcohol such as dizziness and passing out as related to the dosing levels needed to feel the sedative effects of alcohol. Among adolescent and adult samples of both sexes and family-history positive studies of alcoholics,low levels of response, as measured by the SRE have been implicated as a risk factor for alcohol use disorders. This notion that some drinkers need to ingest greater amounts of alcohol to feel its sedative effects and that this effect is related to greater drinking quantities has been recently supported and extended to include the observation that this relationship is also relevant to those reporting lower levels of stimulant effects during the first five drinks. Our finding that negative alcohol experiences were predictive of problem alcohol use is consistent with this research, despite using a different questionnaire, and extends it to include the potential prediction of other drug use problem behaviors.The prevelance of PVCs is increased in patients diagnosed with hypertension especially when it is associated with left ventricular hypertrophy, dilated cardiomyopathy and heart failure,post acute myocardial infarction,and congenital heart disease. PVCs often cause no symptoms. In many patients, the presence of PVCs could result in the sensation of fluttering, pounding, skipped beats, palpitations, dizziness, and/or near syncope. The etiology of PVCs is not well known. Many mechanisms may explain the origin of PVCs, including enhanced normal or abnormal automaticity inside the heart, triggered activity in Purkinje cells of the ventricular myocardium, or reentry. Anxiety, alcohol, caffeine, tobacco, exercise, illicit drugs, hypokalemia, HTN, ischemia, infarction, excessive calcium, drug toxicity,or an underlying heart disease could result in PVCs through previously mentioned mechanisms.
ECG is the mainstay of diagnosis of PVCs. This includes standard ECG, exercise stress ECG, holter monitor, and event recorder depending primarily on the frequency of PVCs which helps to decide the best way to detect them. Only in symptomatic patients do PVCs need to be diagnosed and treated. Beside eliminating previously mentioned possible triggers, beta blockers and calcium channel blockers are recommended as first-line therapy for symptomatic PVCs, especially with outflow tract morphology in a structurally normal heart. Antiarrhythmic medications, such as amiodarone can sometimes be tried but with caution because of its side effects. Frequent PVCs may be associated with worsening of systolic heart failure in patients with a dilated cardiomyopathy. Small studies have suggested that in selected patients, radio frequency ablation of ectopic ventricular foci is associated with an improvement in left ventricular function and clinical improvement in symptoms.The 2006 American College of Cardiology/American Heart Association/European Society of Cardiology guidelines for the management of ventricular arrhythmias included suggestions regarding ablation therapy for PVCs. They note that ablation therapy of PVCs may be useful if they are frequent, symptomatic, and monomorphic, if they are refractory to medical therapy, if the patient chooses to avoid long-term medical therapy, or if they consistently provoke ventricular arrhythmia storm of a similar morphology. SCFP, as a separate entity, has a widely diverse presentation including chest discomfort, unstable angina, non ST elevation MI, ST elevation MI or non-sustained ventricular tachycardia. It usually presents with recurrent rest pain requiring urgent admission. The etiology of SCFP is not completely understood. It is speculated that it is caused by acute but recurrent perturbations of microvascular function. Histopathological examination of left and right ventricular endomyocardial biopsies taken from some patients showed fibromuscular hyperplasia, myofibrilar hypertrophy, endothelial degeneration with swollen endothelial cells encroaching on the lumen, luminal size reduction, mitochondrial abnormalities, lipofuscin deposition, and glycogen content reduction, which can cause the elevation in resting coronary artery resistances, especially toward microvasculature beds, found in SCFP. Normal and pathological zones often coexisted in the same specimen.Thus, in some patients with slow coronary flow and patent coronary arteries, functional obstruction of microvessels seems to be implicated, as it is relieved by dipyridamole infusion.
This shows also that small-vessel CAD can cause classic angina pectoris. The diagnosis can be suspected when the coronary angiogram shows large patent arteries with slow flow of the angiographic contrast medium and it can be confirmed by endomyocardial biopsy. Another study suggested that elevation in plasma homocysteine, evenifitismild,may play a role in the pathogenesis of SCFP by severely disturbing vascular endothelial function and subsequently impairing coronary blood flow, and showed that patients with SCFP have statistically significant raised level of plasma homocysteine compared to control subjects with normal coronary flow.As a treatment, dipyridamole, which has dilatator properties on coronary microvessels, cannabis drying proved to be useful in most patients with SCFP. It abolishes functional obstruction in coronary arteries with diameters less than 200 m and is considered far superior in treating SCFP as compared to nitroglycerine. Other therapies proved to be effective also include simvastatin, atorvastatin, nebivolol, and mibefradil although the use of the latter is limited because of drug interactions caused by its inhibition of the cytochrome P450 3A4 pathway. Beside mean arterial pressure, blood flow in coronary arteries depends on heart contractility. During systole, and because of the big muscular mass of the left ventricle,extravascular compression prevents any antegrade blood flow in left coronary artery particularly at the end of isovolumetric contraction. Conversely, and during diastole and especially early diastole which represents isovolumetric relaxation, coronary blood flow in LCA becomes maximal.In right coronary artery,blood flow is maximal during peak systole, because extravascular compression within the right ventricle is less than its counterpart in the LV preserving antegrade blood flow in RCA in both systole and diastole. The fact that the highest blood flow in LCA occurs throughout different stages of diastole, which is not the case in RCA, assumes that any PVC happening through diastole will have a bigger impact on blood flow in LCA compared to RCA. This, in turn, will be reflected as a slow blood flow in LCA more than in RCA. In patients with SCFP, resting coronary artery resistances, as mentioned above, are abnormally elevated, however, these resistances respond normally to vasodilator stimuli such as papaverine and adenosine and during exercise. Marijuana affects the heart in different ways. The acute cardiovascular effects of marijuana, which are palpitations, tachycardia, elevated blood pressure, and a greater myocardial oxygen demand, are mainly caused by increased release of catecholamines. Chronic use of marijuana can worsen any underlying disease through prolonged vasoconstriction and causes digital clubbing.After a thorough review of the literature, it was noted that there was a lack of description of any specific time frame, after which marijuana consumption will have effects on the heart, resulting in myocardial ischemia or heart failure. Patient’s age and the presence of underlying CAD are key players in determining how fastthe results of smoking marijuana will take effect on the heart, especially when it comes to chronic use. The mechanisms by which marijuana affects the heart are diverse including increased cardiac work through elevated catecholamines and carboxyhemoglobin levels, as well as possible episodes of intense postural hypotension. Moreover, smoking cannabis was rarely found to trigger MI. Among cannabis users who sustained an acute MI, the risk was nearly five times higher within the first hour after smoking compared to periods of nonuse.