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Also we’ve had some new combinations appear and basically we have three of those, and I won’t go into them in great detail. There’s TARKA, LEXO and TEXAM, and basically they are all ACE I inhibitors plus a calcium channel blocker. These drugs may be useful in patients with diabetes, hyperlipidemia, hyperuricemia as those parameters don’t seem to be altered by this combination of medications.
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With regard to smoking cessation, you may or may not have heard of the drug Zyban, which is basically Wellbutrin online, an antidepressant repackaged. This is given in a dose of 150 mg twice a day. It seems to help with the curbing of the urge for the smokers. In one respect it’s better than using nicotine substitutes in that in case your patients exhibit their human frailties and backslide, and start smoking, this medication will not lead them to nicotine excess like the patches or the gums, and they can, in fact, smoke for the first four or five days when they start this medication as they begin to lose their urge. They can continue to smoke and not experience the adverse effects, but long-term it still takes a very active role, as far as the practitioners and your office staff to keep the patient from smoking.
The role of family practice in the acute intervention of myocardial events has changed a lot. However, we all still need to be very attuned to this problem because you never know what’s behind door number three. When you go down the hall and you begin to go into a room that is maybe there for stomach pain – sometimes patients make the wrong diagnosis, and it’s not their stomach at all. Therefore right from the office sometimes we can be faced with and acute cardiac event.
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Thrombolytic therapy in this city is pretty unusual. We have a very aggressive and competent force of cardiologists here in this town and basically from door to Cath Lab can be an hour. And I think that is the goal here. For those of our colleagues that practice in more remote areas, thrombolytics still play an important role in how they manage their patients and need to be utilized because a potentially life-saving benefit of these drugs is still very significant. However, as a family physician, it is still pertinent for me to know that when I send my patient to the Emergency Room, or if I see them in the office and I’m going to take them over there directly, that I can make a difference in their overall outcome with aspirin. I keep a bottle of aspirin in the office. It’s cheap, it’s got a long shelf life, it can do a lot of good. Once a patient is in the Emergency Room, while I’m waiting for my cardiology consultation, if I think the patient is experiencing unstable angina or an acute event, it’s a good idea to start a heparin drip. We also tend to use an IV beta-blocker if the underlying heart rate permits. These three simple steps can reduce recurrent ischemic events until something definitive happens. Either the event ceases, something is done on an acute basis, for example a Cath Lab usually, or the event completes itself.

Then there is also the consideration of co-morbid conditions. There is a category of compelling indications in this last series of recommendations. For example, diabetics with proteinuria. There’s a strong indication for using ACE inhibitors. For patients who have also the co-morbid condition of heart failure, consider ACE inhibitors and diuretics. Isolated systolic hypertension, especially in older patients, diuretics and probably long-acting dihydropyridine calcium channel blockers. Those patients who have experienced myocardial infarction, you heard about the benefit of beta-blockers, especially those without the ISA, or intrinsic sympathomimetic activity, and then the ACE inhibitors especially in those post-MI patients with systolic dysfunction.
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Now in the last year, year or two, we have seen one new beta-blocker enter the arena and that is cheap Coreg, curvediol. It’s a non-selective beta-blocker and it’s indicated for both hypertension and congestive heart failure. This is pretty remarkable when you think about five or six years ago we all stood back and said, “Um, beta-blocker? Congestive heart failure? I don’t think that’s a healthy combination and we don’t want to do that.” But with the non-selectivity, that kind of opens the door for the use here. It seems to also be beneficial in ischemic and non-ischemic heart failure, however it’s still a beta-blocker and it will lower heart rate so it’s probably best to avoid it in those patients with significant underlying bradycardia. Unfortunately, it is also a b.i.d. drug and that may lower compliance a little bit.
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In the ACE arena we’ve seen the appearance of the ACE II inhibitors and the most recent one is Diovan, which is valsartan. It’s similar to the losartan, which was the first entry, and that was Cozaar. The valsartan seemed to be very similar in efficacy to the other ACE inhibitors but there seems to be less causative effect to that dry, hacking cough, and the valsartan seems to be more efficacious in all comers as far as gender, race, sex. Some of the ACE I blockers did not seem to be very effective in black patients. In addition, this valsartan is priced competitively with the other ACE inhibitors. I personally think that this is going to be a very interesting drug category to watch. Right now it’s a little bit different from ACE I inhibitors, but it’s once a day, it seems to cause less side effects and I’ll be very interested to see if in the next two or three years if the ACE II class doesn’t in fact sort of replace the ACE I class.

In the calcium channel blocker classification, we have a new subgroup of calcium channel blockers, the tetralol group. Right now there’s only one that we are using and that’s the Posicor. It’s recommended for both high blood pressure and angina and it has the interesting effect that it may also slow heart rate. Some of the early calcium channel blockers had the reflex tachycardia and we don’t seem to see that with the Posicor. Unfortunately it is also subject to the interaction that you heard about earlier with the statin drugs as it is metabolized through the cytochrome P450 enzyme channel.

Cholesterol. I want to talk about some of the new things that have become available to us. Baycol is an HMG co-A reductase inhibitor. It’s Cerivastatin. It does reduce cholesterol, both total cholesterol and LDL cholesterol, and with the recommended dosage it can probably reach that 20 -25% reduction that you heard was probably significant. It does require monitoring of the liver function tests like the other statins and like the other statins you have to be acute and chronically aware of the potential interactions with other medications. At this point in time, it probably does not have any apparent significant advantage over the other statins.
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The other statin that I wanted to briefly mention was Lipitor, or atorvastatin. This drug seems to have a very potent initial response, as far as lower total cholesterol, LDL and triglycerides. When you look at how this drug stacks up against the other statins, the lowest dose of this drug appears to reduce the LDL and cholesterol in an equivalent measure with the upper level doses of the other statins. It can even apparently reduce LDL’s up to 40%. Now whether or not that’s going to be the crucial number that we heard about this morning, or not. If we reduce LDL’s by 24% from their starting point, that too can be an adequate endpoint.

The Joint National Committee on prevention, detection, evaluation and treatment of high blood pressure (JNC VI). Over the years with the different JNC trials we’ve seen the pendulum swing back and forth as far as what’s the first choice of medication for high blood pressure. And now we are back to where we were probably ten or 12 years ago as far as diuretics and beta-blockers. Now as I read through this last JNC recommendation, probably the most significant difference is that they are loosening up and liberalizing a little bit, with regard to the use of combination drugs. Several years ago we used to have what was called the “step” therapy approach. You pay your money, you take your choice for the first drug and then you push it to the limits of the dosage and then if you don’t get success you add on another drug, and on up the tier to whatever it takes to control the patient. Now the recommendations have loosened up a little bit, and they do recognize that using a combination drug earlier in the course of therapy may actually be more worthwhile, in that you decrease side effect potential from maximizing the dose of one drug and that sometimes 1 plus 1 equals 3, when you are talking about the efficacy of the medications.
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Then there are a number of other things that include adding triamatharmaline, adding stimulant to another drug ongoing. These are things that are maybe worth trying in individual cases empirically with the research data supporting these. The SSRIs are very helpful and useful in major depression but in severe anxiety disorders, in OCD, in attention deficit disorder, in eating disorders. Perhaps they may help with certain chronic pain syndromes although SSRIs, in fact, are less useful there. Especially the really old tertiary tricyclics were particularly good in diabetic neuropathy and certain other chronic pain syndromes for reasons that we don’t understand. But the point being that there are many panic disorders, enuresis and there are many other indications for antidepressants and that’s really good news.
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Then finally I would have said a bit about where we are in our understanding long term maintenance therapy of antidepressants and I can summarize that very quickly by saying that in my mind the jury is still out and you have to be careful how you discuss this at the board exams because the parting line is that there is a lot of evidence that long term maintenance therapy is a good thing, the longer the better, the more aggressive the better. The problem for me in that literature is that most of that literature contrasts persons kept on drug and then people randomized to come off rather abruptly with placebo. I can tell you that going from treated to untreated, especially abruptly, is not a nice thing to do to people and we’ve proven this now with lithium and bipolar illness, neuroleptics and schizophrenia and I strongly suspect, I can’t prove it yet, that it’s a dangerous thing to do in apparently recovered depressed persons.
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Our recent quantitative meta-analysis of that literature showed that you can predict who is likely to fail. Sooner after recovery probably higher risk and most people in practice would keep up continuation therapy for at least six to twelve months after apparent recovery. When you go beyond the year followup, the data are less convincing.
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If you have had a larger number of episodes or if you have a chronic dysthymic or depressive disorder, your likelihood of relapse a year, 2 years, 3 years out goes up and it’s a quantitative risk relationship. The more episodes, the greater the likelihood of risk when you come off. However, on treatment past history doesn’t matter as much to the likelihood of response and that’s good news. So even persons who have had many episodes or have chronic depressions, long term therapy can be very helpful and past history matters less, the treatment response matters a great deal and risk of getting sick again if you stop, particularly, abruptly.